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1.
  • Andreasson, Anna, et al. (författare)
  • A global measure of sickness behaviour : Development of the Sickness Questionnaire
  • 2018
  • Ingår i: Journal of Health Psychology. - : SAGE Publications. - 1359-1053 .- 1461-7277. ; 23:11, s. 1452-1463
  • Tidskriftsartikel (refereegranskat)abstract
    • Symptoms after inflammatory activation, so-called sickness behaviour, overlap with trans-diagnostic complaints. As no self-report questionnaire to assess sickness behaviour exists, we aimed to develop such an instrument, the Sickness Questionnaire. Items responsive to experimentally induced inflammatory activation (randomized double-blind study endotoxin (0.6 ng/kg) versus placebo, n = 52) were selected and the statistical properties were examined in 172 primary care patients. A principal component analysis indicated a one-factor solution (Cronbach's alpha = .86). This 10-item scale correlated with depression ( β = .41, p < .001), anxiety ( β = .36, p < .001), self-rated health ( β = .28, p < .001) and a single item of feeling sick ( β = .55, p < .001). The results support the adequacy of Sickness Questionnaire as a brief assessment instrument of perceived sickness behaviour.
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2.
  • Andreasson, Anna, et al. (författare)
  • The effect of a transient immune activation on subjective health perception in two placebo controlled randomised experiments
  • 2019
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 14:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Patient-reported outcomes predict mortality and play increasingly important roles in care, but factors that modify central measures such as health ratings have been little investigated. Building on designated immune-to-brain pathways, we aimed to determine how a short-term induced inflammation response impacts self-reported health status. Methods Lipopolysaccharide injections were used to provoke acute systemic inflammatory responses in healthy men and women and were compared to placebo in two double-blind randomized experiments. In Experiment 1, 8 individuals (mean 24 years; SD = 3.7) received lipopolysaccharide 0.8 ng/kg once and placebo once in a cross-over design, and in Experiment 2, 52 individuals received either lipopolysaccharide 0.6 ng/kg or placebo once (28.6 years; SD = 7.1). Main outcomes were perceived health (general and current), sickness behaviour (like fatigue, pain and negative affect), and plasma interleukin-6, interleukin-8 and tumour necrosis factor-alpha, before and after injection. Results Compared to placebo, lipopolysaccharide lead to a deterioration in both self-rated general (Experiment 1, b = 1.88 for 0.8 ng/kg) and current health (Experiment 1 b = -3.00; and Experiment 2 b = -1.79) 1.5h after injection (p's<0.01), effects that remained after 4.5 to 5 hours (p's<0.05). The effect on current health in Experiment 2 was mediated by increased inflammation and sickness behaviour in response to lipopolysaccharide injection (beta = -0.28, p = 0.01). Conclusion Health is drastically re-evaluated during inflammatory activation. The findings are consistent with notions that inflammation forms part of health-relevant interoceptive computations of bodily state, and hint at one mechanism as to why subjective health predicts longevity.
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3.
  • Gordon, Amy R., et al. (författare)
  • Detection of Inflammation via Volatile Cues in Human Urine
  • 2018
  • Ingår i: Chemical Senses. - : Oxford University Press (OUP). - 0379-864X .- 1464-3553. ; 43:9, s. 711-719
  • Tidskriftsartikel (refereegranskat)abstract
    • Contagious disease is a major threat to survival, and the cost of relying on the immune system to defeat pathogens is high; therefore, behavioral avoidance of contagious individuals is arguably an adaptive strategy. Animal findings demonstrate the ability to detect and avoid sick individuals by the aid of olfactory cues, and a recent study indicated that human axillary odor also becomes more aversive as a function of immune activation. By injecting healthy human participants with lipopolysaccharide (0.6 ng/kg body weight) to experimentally induce inflammation, this study demonstrates that natural daily rhythms of urine odor-its perceived dimensions and volatile profile-are altered within hours of inflammation onset. Whereas healthy human urine decreases in averseness over the course of a single day, inflammation interrupts this process and results in an increased urine odor averseness and an altered volatile composition. These results support the notion that subtle and early cues of sickness may be detected and avoided, thereby complementing the immune system in its role of keeping us alive and healthy.
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4.
  • Gordon, Amy R., et al. (författare)
  • Human scent as a first-line defense against disease
  • 2023
  • Ingår i: Scientific Reports. - : Springer Nature. - 2045-2322. ; 13:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Individuals may have a different body odor, when they are sick compared to healthy. In the non-human animal literature, olfactory cues have been shown to predict avoidance of sick individuals. We tested whether the mere experimental activation of the innate immune system in healthy human individuals can make an individuals' body odor be perceived as more aversive (intense, unpleasant, and disgusting). Following an endotoxin injection (lipopolysaccharide; 0.6 ng/kg) that creates a transient systemic inflammation, individuals smelled more unpleasant compared to a placebo group (saline injection). Behavioral and chemical analyses of the body odor samples suggest that the volatile components of samples from sick individuals changed qualitatively rather than quantitatively. Our findings support the hypothesis that odor cues of inflammation in axillary sweat are detectable just a few hours after experimental activation of the innate immune system. As such, they may trigger behavioral avoidance, hence constituting a first line of defense against pathogens of infected conspecifics.
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5.
  • Gordon, Amy R., et al. (författare)
  • The scent of disease
  • 2015
  • Ingår i: Chemical Senses. - : Oxford University Press (OUP). - 0379-864X .- 1464-3553. ; 40:3, s. 254-254
  • Tidskriftsartikel (refereegranskat)abstract
    • Ability to detect diseases in conspecifics would be advantageous for the individual. In line with this, rodents avoid body odors of infected individuals. Two studies (Olsson et al. 20014; in prep.) indicated that this is possible by way of human smell and human observers. T-shirts from donors (worn for 4 hours) that had received an injection of endotoxin [0.8ng lipopolysaccharide (LPS) / kg body weight], which causes systemic inflammation, smelled more unpleasant, intense, and sick than shirts from donors that had received a placebo (Saline) injection. GC/MS analysis of the shirts suggested that the change of body odor was not due to a general increase of odorous compounds in the “sick shirts” compared to “placebo shirts” but rather to a qualitative change. Study 2 (ongoing) further investigated the nature of this perception. In a first experiment, we compared the body odor of 30 endotoxin (0.6ng LPS / kg body weight) and 21 placebo (Saline) donors. Again, body odors were sampled during 4 hours using T-shirts. Observers then smelled the shirts and rated intensity, pleasantness, and disgust. In a second experiment, urine from these donors were collected and was investigated in the same way with subjective ratings. Altogether the data suggest that systemic inflammation makes body odors more aversive within a few hours.
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6.
  • Hedman, Erik, et al. (författare)
  • Health anxiety in a disease-avoidance framework : Investigation of anxiety, disgust and disease perception in response to sickness cues
  • 2016
  • Ingår i: Journal of Abnormal Psychology. - : American Psychological Association (APA). - 0021-843X .- 1939-1846. ; 125:7, s. 868-878
  • Tidskriftsartikel (refereegranskat)abstract
    • Severe health anxiety is characterized by a debilitating fear of somatic illness, and avoidance of disease-related stimuli plays a key role in the maintenance of the disorder. The aim of this study was to investigate severe health anxiety within an evolutionary disease-avoidance framework. We hypothesized that, compared to healthy controls, participants with severe health anxiety would perceive others as sicker, more contagious, and less attractive. We also expected individuals with severe health anxiety to be more prone to avoid interaction with persons who appeared sick, as well as to respond with more health-related worry, more disgust, and more anxiety when confronting such individuals. In addition, this sensitivity was expected to be larger if people showed manifest sickness symptoms. Participants with and without severe health anxiety (N = 224) were exposed to facial photos with a varying degree of apparent sickness. Patients with severe health anxiety, compared to controls, rated apparently healthy people as being less healthy and less attractive. There were significant interaction effects showing that that the increase in disgust, anxiety, perceived contagiousness, and worry over one's own health as a function of how sick the person in the photo appeared, was significantly larger in the clinical sample compared to the healthy control sample (ps < .047). Results from regression analyses using health anxiety as a dimensional predictor also supported our hypotheses. We suggest that disgust and cognitive biases relating to the disease-avoidance model are significant features of severe health anxiety. (PsycINFO Database Record
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7.
  • Jonsjö, Martin A., et al. (författare)
  • Patients with ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) and chronic pain report similar level of sickness behavior as individuals injected with bacterial endotoxin at peak inflammation
  • 2020
  • Ingår i: Brain, Behavior, & Immunity - Health. - : Elsevier BV. - 2666-3546. ; 2
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Chronic sickness behavior is implicated in ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) and chronic pain but the level of subjective sickness behavior in these conditions has not been investigated or compared to other clinical and non-clinical samples, or to the level in experimental inflammation. Furthermore, the relationship between sickness behavior and self-rated health and functioning is not known in patients with ME/CFS and chronic pain. The aim of the present study was to investigate how sickness behavior in patients with chronic conditions differs from that in individuals with experimental acute sickness, primary care patients, the general population and healthy subjects. In addition, we wanted to explore how sickness behavior is related to self-rated health and health-related functioning.Methods: Sickness behavior was quantified using the sickness questionnaire (SicknessQ). Self-ratings were collected at one time-point in 6 different samples. Levels of sickness behavior in patients with ME/CFS (n ​= ​38) and patients with chronic pain (n ​= ​190) were compared to healthy subjects with lipopolysaccharide(LPS)-induced inflammation (n ​= ​29), primary care patients (n ​= ​163), individuals from the general population (n ​= ​155) and healthy subjects (n ​= ​48), using linear regression. Correlations and moderated regression analyses were used to investigate associations between sickness behavior and self-rated health and health-related functioning in ME/CFS, chronic pain and the general population.Results: LPS-injected individuals (M ​= ​16.3), patients with ME/CFS (M ​= ​16.1), chronic pain (M ​= ​16.1) and primary care patients (M ​= ​10.7) reported significantly higher SicknessQ scores than individuals from the general population (M ​= ​5.4) and healthy subjects (M ​= ​3.6) all p’s ​< ​0.001). In turn, LPS-injected individuals, patients with ME/CFS and chronic pain reported significantly higher SicknessQ scores than primary care patients (p’s ​< ​0.01). Higher levels of sickness behavior were associated with poorer self-rated health and health-related functioning (p’s ​< ​0.01), but less so in patients with ME/CFS and chronic pain than in individuals from the general population.Conclusions: Patients with ME/CFS and chronic pain report similar high levels of sickness behavior; higher than primary care patients, and comparable to levels in experimental inflammation. Further study of sickness behavior in ME/CFS and chronic pain populations is warranted as immune-to-brain interactions and sickness behavior may be of importance for functioning as well as in core pathophysiological processes in subsets of patients.
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8.
  • Karshikoff, Bianka, et al. (författare)
  • Baseline Pro-Inflammatory Cytokine Levels Moderate Psychological Inflexibility in Behavioral Treatment for Chronic Pain
  • 2022
  • Ingår i: Journal of Clinical Medicine. - : MDPI AG. - 2077-0383. ; 11:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The medical and scientific communities struggle to understand chronic pain and find effective treatments. Multimodal approaches are encouraging but show significant individual differences. Methods: Seventy-eight persons (56 women) with chronic pain received Acceptance and Commitment Therapy and provided blood samples before and after treatment. The participants completed surveys with the blood sampling. Blood plasma was analyzed for IL-6 and TNF-α levels with the Olink Inflammation Panel (Olink Bioscience Uppsala, Sweden). The treatment effects and moderating effects of low-grade inflammation on changes in outcomes were analyzed using linear mixed models. Results: Pain interference (p < 0.001) and psychological inflexibility (p < 0.001) improved significantly during treatment, but pain intensity did not (p = 0.078). Cytokine levels did not change over the course of the treatment (IL-6/TNF-α p = 0.086/0.672). Mean baseline levels of IL-6 and TNF-α moderated improvement in psychological inflexibility during the course of treatment (p = 0.044), but cytokine levels did not moderate changes in pain interference (p = 0.205) or pain intensity (p = 0.536). Conclusions: Higher baseline inflammation levels were related to less improvement in psychological inflexibility. Low-grade inflammation may be one factor underlying the variability in behavioral treatment in chronic pain.
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9.
  • Karshikoff, Bianka, et al. (författare)
  • Editorial : Vulnerability and protective factors for inflammation-associated somatoform and mental disorders
  • 2022
  • Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 106, s. 227-230
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Over the past 30 years, research in psychoneuroimmunology and immunopsychiatry points to immune processes playing a part in the development and maintenance of various non-communicable disorders, including chronic pain (Grace et al., 2014), chronic fatigue (Lacourt et al., 2018), depression (Zunszain et al., 2013), anxiety (Michopoulos et al., 2016), psychosis (Ullah et al., 2021) and neurodegeneration (Park et al., 2020). Many of these disorders are characterized by a complex symptomatology, various comorbidities, and a difficulty to treat the disorder satisfactorily. Although recent research shows that immune alterations and inflammatory components may contribute to the pathophysiology of these diseases, inflammation is probably not sufficient to independently induce these disorders or maintain them. Not all individuals with a heightened inflammatory activity will develop one of these disorders, and some individuals with these disorders show no changes in immune parameters. This suggests the involvement of additional factors that interact with the immune system to cause vulnerability to, or a protection against, inflammation-associated disorders.In this special issue of Brain, Behavior and Immunity, we welcomed articles investigating predictors and moderators of inflammation-associated disorders, comorbidities, and behavioral changes. The studies included in this issue range from experimental human and animal studies to clinical investigations applying proteomic approaches. The disorders discussed include those related to aging and neurodegenerative diseases, psychiatric disorders, fatigue, and pain. The authors contributing to this special issue tackle some fundamental questions, including: Why do not all individuals with a heightened inflammatory activity develop one of these disorders? How can we protect against the neuropsychiatric effects of inflammation? Does inflammation interact with other pathological processes of clinical conditions such as Parkinson’s disease and Alzheimer’s disease?
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10.
  • Karshikoff, Bianka, et al. (författare)
  • Inflammatory Blood Signature Related to Common Psychological Comorbidity in Chronic Pain
  • 2023
  • Ingår i: Biomedicines. - : MDPI. - 2227-9059. ; 11:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic pain is characterized by high psychological comorbidity, and diagnoses are symptom-based due to a lack of clear pathophysiological factors and valid biomarkers. We investigate if inflammatory blood biomarker signatures are associated with pain intensity and psychological comorbidity in a mixed chronic pain population. Eighty-one patients (72% women) with chronic pain (>6 months) were included. Patient reported outcomes were collected, and blood was analyzed with the Proseek Multiplex Olink Inflammation Panel (Bioscience Uppsala, Uppsala, Sweden), resulting in 77 inflammatory markers included for multivariate data analysis. Three subgroups of chronic pain patients were identified using an unsupervised principal component analysis. No difference between the subgroups was seen in pain intensity, but differences were seen in mental health and inflammatory profiles. Ten inflammatory proteins were significantly associated with anxiety and depression (using the Generalized Anxiety Disorder 7-item scale (GAD-7) and the Patient Health Questionnaire (PHQ-9): STAMBP, SIRT2, AXIN1, CASP-8, ADA, IL-7, CD40, CXCL1, CXCL5, and CD244. No markers were related to pain intensity. Fifteen proteins could differentiate between patients with moderate/high (GAD-7/PHQ-9 > 10) or mild/no (GAD-7/PHQ-9 < 10) psychological comorbidity. This study further contributes to the increasing knowledge of the importance of inflammation in chronic pain conditions and indicates that specific inflammatory proteins may be related to psychological comorbidity.
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11.
  • Karshikoff, Bianka, et al. (författare)
  • Role of inflammation in Human Fatigue : Relevance of Multidimensional Assessments and Potential Neuronal Mechanisms
  • 2017
  • Ingår i: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 8
  • Forskningsöversikt (refereegranskat)abstract
    • Fatigue is a highly disabling symptom in various medical conditions. While inflammation has been suggested as a potential contributor to the development of fatigue, underlying mechanisms remain poorly understood. In this review, we propose that a better assessment of central fatigue, taking into account its multidimensional features, could help elucidate the role and mechanisms of inflammation in fatigue development. A description of the features of central fatigue is provided, and the current evidence describing the association between inflammation and fatigue in various medical conditions is reviewed. Additionally, the effect of inflammation on specific neuronal processes that may be involved in distinct fatigue dimensions is described. We suggest that the multidimensional aspects of fatigue should be assessed in future studies of inflammation-induced fatigue and that this would benefit the development of effective therapeutic interventions.
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12.
  • Karshikoff, Bianka (författare)
  • Sickness behavior : immune system influences on brain and behavior
  • 2015
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Sickness behavior is a motivational state that redirects the needs and priorities of the organism during infection to aid recovery. The behavioral changes include fatigue, lowered mood and aches. Peripheral cytokines signal to the brain via autonomic nerves and the bloodbrain interface and change the inflammatory status of the brain, a mechanism that in recent years has been implied in complex syndromes like long-term pain, depression, fatigue and overall poor well-being. Epidemiological studies also suggest that chronic inflammatory disease like allergy increases the risk of developing Alzheimer disease (AD) later in life. In this thesis we explored how acute experimental immune activation affects pain sensitivity and self-rated general health. We also investigated inflammatory and degenerative effects in the brain following chronic allergic inflammation in a mouse model. In Paper I, eight healthy participants (1 woman) were injected with 0.8 ng/kg body weight lipopolysaccharide (LPS) and with saline 28 days apart in a balanced double-blind withinsubject design. Subsequently, 52 subjects were injected with 0.6 ng/kg LPS (31, 18 women) or saline (21, 11 women) in a double-blind between-subject design (data from this protocol was also used for Paper II and IV). Pro-inflammatory peripheral cytokine (TNF- α, IL-6 and IL-8) levels increased significantly in the LPS group. We demonstrated that in particular deep pain sensitivity increased during immune activation. Women were more affected than men by the inflammatory signals with regard to pain, as women also demonstrated increased cutaneous pain sensitivity and impaired descending pain inhibition during LPS provocation, whereas men did not. Pain sensitivity was associated with peripheral IL-6 and IL-8 levels for both men and women. In Paper II (second sample in Paper I), we investigated the neural correlates underlying these findings, using functional magnetic resonance imaging. LPS attenuated descending endogenous pain inhibition reflected as decreased activity in the rostral anterior cingulate (rACC) and lateral prefrontal cortices. Also, the LPS group demonstrated increased insular activity, which may reflect amplified interoceptive and/or affective processing. An overall weaker pain regulation (lower rACC activity) and an association between insular activation and peripheral pro-inflammatory cytokines were found in women, which may explain the sex differences found in pain sensitivity. The higher susceptibility to inflammation-driven pain sensitivity in women may be one of the mechanisms behind more women suffering from pain conditions. In Paper III we studied the impact of long-term peripheral inflammation on inflammatory and neurodegenerative processes in the brain. We used a murine model for chronic allergic inflammation by ovalbumin provocation and assessed AD and inflammation relevant markers. We showed that chronic allergic inflammation induces tau-phosphorylation in mice, a hallmark of AD. Also, chronic inflammation resulted in antibody increases (IgG and IgE) in the mouse brain, which in turn could lead to neuroinflammation over time. In Paper IV (same sample as Paper II) we assessed self-rated general health (SRH) and subjective sickness behavior during the peak of the peripheral inflammatory response. We showed that SRH ratings worsened markedly during experimental inflammation, and that these effects were statistically mediated by the symptoms of sickness behavior perceived by the subjects. In conclusion, our findings corroborate related clinical research findings, suggesting that the inflammatory models used in this thesis may serve as useful tools for studying neuroimmune mechanisms relevant for chronic pain, neurodegeneration and states characterized by poor subjective health. A better understanding of sickness-induced brain changes may aid future treatment strategies for such complex diseases that currently often lack successful treatment.
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13.
  • Karshikoff, Bianka, et al. (författare)
  • Why sickness hurts : A central mechanism for pain induced by peripheral inflammation
  • 2016
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 57, s. 38-46
  • Tidskriftsartikel (refereegranskat)abstract
    • Low-grade systemic inflammation has been implicated in chronic pain, as well as in comorbid diseases like depression and fatigue. We have previously shown that women's pain perception and regulation is more affected by systemic inflammation than that of men. Here we investigated the neural substrates underlying these effects using an fMRI paradigm previously employed in a clinical population. Fifty-one participants (29 women) were injected with 0.6ng/kg lipopolysaccharide (LPS) or saline to induce a peripheral inflammatory response. The subjects were then tested with a pressure pain fMRI paradigm designed to capture descending pain inhibitory activity 2h after injection, and blood was sampled for cytokine analysis. The subjects injected with LPS became more pain sensitive compared to the placebo group, and the heightened pain sensitivity was paralleled by decreased activity in the ventrolateral prefrontal cortex and the rostral anterior cingulate cortex (rACC) compared to placebo; areas involved in descending pain regulation. The LPS group also had higher activity in the anterior insular cortex, an area underpinning affective and interoceptive pain processing. Women displayed overall less pain-evoked rACC activity compared to men, which may have rendered women less resilient to immune provocation, possibly explaining sex differences in LPS-induced pain sensitivity. Our findings elucidate the pain-related brain circuits affected by experimental peripheral inflammation, strengthening the theoretical link between systemic inflammation and weakened pain regulation in chronic pain disorders. The results further suggest a possible mechanism underlying the female predominance in many chronic pain disorders.
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14.
  • Lasselin, Julie, et al. (författare)
  • Comparison of bacterial lipopolysaccharide-induced sickness behavior in rodents and humans : Relevance for symptoms of anxiety and depression
  • 2020
  • Ingår i: Neuroscience and Biobehavioral Reviews. - : Elsevier BV. - 0149-7634 .- 1873-7528. ; 115, s. 15-24
  • Forskningsöversikt (refereegranskat)abstract
    • Increasing evidence from animal and human studies suggests that inflammation may be involved in mood disorders. Sickness behavior and emotional changes induced by experimental inflammatory stimuli have been extensively studied in humans and rodents to better understand the mechanisms underlying inflammationdriven mood alterations. However, research in animals and humans have remained compartmentalized and a comprehensive comparison of inflammation-induced sickness and depressive-like behavior between rodents and humans is lacking. Thus, here, we highlight similarities and differences in the effects of bacterial lipopolysaccharide administration on the physiological (fever and cytokines), behavioral and emotional components of the sickness response in rodents and humans, and discuss the translational challenges involved. We also emphasize the differences between observable sickness behavior and subjective sickness reports, and advocate for the need to obtain both subjective reports and objective measurements of sickness behavior in humans. We aim to provide complementary insights for translational clinical and experimental research on inflammation-induced behavioral and emotional changes, and their relevance for mood disorders such as depression.
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15.
  • Lasselin, Julie, et al. (författare)
  • Fatigue and sleepiness responses to experimental inflammation and exploratory analysis of the effect of baseline inflammation in healthy humans
  • 2020
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 83, s. 309-314
  • Tidskriftsartikel (refereegranskat)abstract
    • Inflammation is believed to be a central mechanism in the pathophysiology of fatigue. While it is likely that dynamic of the fatigue response after an immune challenge relates to the corresponding cytokine release, this lacks evidence. Although both fatigue and sleepiness are strong signals to rest, they constitute distinct symptoms which are not necessarily associated, and sleepiness in relation to inflammation has been rarely investigated. Here, we have assessed the effect of an experimental immune challenge (administration of lipopolysaccharide, LPS) on the development of both fatigue and sleepiness, and the associations between increases in cytokine concentrations, fatigue and sleepiness, in healthy volunteers. In addition, because chronic-low grade inflammation may represent a risk factor for fatigue, we tested whether higher baseline levels of inflammation result in a more pronounced development of cytokine-induced fatigue and sleepiness. Data from four experimental studies was combined, giving a total of 120 subjects (LPS N = 79, 18 (23%) women; Placebo N = 69, 12 (17%) women). Administration of LPS resulted in a stronger increase in fatigue and sleepiness compared to the placebo condition, and the development of both fatigue and sleepiness closely paralleled the cytokine responses. Individuals with stronger increases in cytokine concentrations after LPS administration also suffered more from fatigue and sleepiness (N = 75), independent of gender. However, there was no support for the hypothesis that higher baseline inflammatory markers moderated the responses in fatigue or sleepiness after an inflammatory challenge. The results demonstrate a tight connection between the acute inflammatory response and development of both fatigue and sleepiness, and motivates further investigation of the involvement of inflammation in the pathophysiology of central fatigue.
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16.
  • Lasselin, Julie, et al. (författare)
  • Lipopolysaccharide Alters Motivated Behavior in a Monetary Reward Task : a Randomized Trial
  • 2017
  • Ingår i: Neuropsychopharmacology. - : Springer Science and Business Media LLC. - 0893-133X .- 1740-634X. ; 42:4, s. 801-810
  • Tidskriftsartikel (refereegranskat)abstract
    • Inflammation-induced sickness is associated with a large set of behavioral alterations; however, its motivational aspects remain poorly explored in humans. The present study assessed the effect of lipopolysaccharide (LPS) administration at a dose of 2 ng/kg of body weight on motivation in 21 healthy human subjects in a double-blinded, placebo (saline)-controlled, cross-over design. Incentive motivation and reward sensitivity were measured using the Effort Expenditure for Rewards Task (EEfRT), in which motivation for high-effort/high-reward trials vs low-effort/low-reward trials are manipulated by variations in reward magnitude and,probability to win. Because of the strong interactions between sleepiness and motivation, the role of sleepiness was also determined. As expected, the probability to win predicted the choice to engage in high-effort/high-reward trials; however, this occurred at a greater extent after LPS than after saline administration. This effect was related to the level of sleepiness. Sleepiness increased motivation to choose the high-effort/high-reward mode of response, but only when the probability to win was the highest. LPS had no effect on reward sensitivity either directly or via sleepiness. These results indicate that systemic inflammation induced by LPS administration causes motivational changes in young healthy subjects, which are associated with sleepiness. Thus, despite its association with energy-saving behaviors, sickness allows increased incentive motivation when the effort is deemed worthwhile.
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17.
  • Lasselin, Julie, et al. (författare)
  • Mood disturbance during experimental endotoxemia : Predictors of state anxiety as a psychological component of sickness behavior
  • 2016
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 57, s. 30-37
  • Tidskriftsartikel (refereegranskat)abstract
    • Lipopolysaccharide (LPS) administration is a well-established model to assess afferent immune-to-brain communication and behavioral aspects of inflammation. Nevertheless, only few studies in comparatively small samples have assessed state anxiety as a psychological component of sickness behavior despite possible clinical implications for the pathophysiology of neuropsychiatric conditions. Thus, the goal of the present analyses carried out in a large, pooled dataset from two independent study sites was to analyze the state anxiety response to LPS administration and to investigate predictors (i.e., cytokine changes; pre-existing anxiety and depression symptoms assessed with the Hospital Anxiety and Depression Scale) of the LPS-induced state anxiety changes at different time points after LPS administration. Data from 186 healthy volunteers who participated in one of six randomized, placebo-controlled human studies involving intravenous administration of LPS at doses of 0.4-0.8ng/kg body weight were combined. State anxiety as well as circulating interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-10 concentrations were significantly increased 2h and 3h after LPS administration, with a peak at 2h, and returned to baseline 6h after administration. Greater changes in IL-6 from baseline to 3h after LPS administration significantly and independently predicted a more pronounced LPS-induced state anxiety response. In addition, higher pre-existing subclinical anxiety symptoms significantly predicted a lower increase in state anxiety 3h and 6h after LPS-administration, which was mediated by TNF-α changes. In conclusion, our findings give additional support for a putative role of inflammatory mechanisms in the pathophysiology of stress-related and anxiety disorders and give new insight on the potential role of pre-existing subclinical affective symptoms.
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18.
  • Lasselin, Julie, et al. (författare)
  • Sex differences in how inflammation affects behavior : What we can learn from experimental inflammatory models in humans
  • 2018
  • Ingår i: Frontiers in neuroendocrinology (Print). - : Elsevier BV. - 0091-3022 .- 1095-6808. ; 50, s. 91-106
  • Forskningsöversikt (refereegranskat)abstract
    • Human models demonstrate that experimental activation of the innate immune system has profound effects on brain activation and behavior, inducing fatigue, worsened mood and pain sensitivity. It has been proposed that inflammation is a mechanism involved in the etiology and maintenance of depression, chronic pain and long-term fatigue. These diseases show a strong female overrepresentation, suggesting that a better understanding of sex differences in how inflammation drives behavior could help the development of individualized treatment interventions. For this purpose, we here review sex differences in studies using experimental inflammatory models to investigate changes in brain activity and behavior. We suggest a model in which inflammation accentuates sex differences in brain networks and pre-existing vulnerability factors. This effect could render women more vulnerable to the detrimental effects of immune-to-brain communication over time. We call for systematic and large scale investigations of vulnerability factors for women in the behavioral response to inflammation.
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19.
  • Lekander, Mats, et al. (författare)
  • Intrinsic functional connectivity of insular cortex and symptoms of sickness during acute experimental inflammation
  • 2016
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 56, s. 34-41
  • Tidskriftsartikel (refereegranskat)abstract
    • Task-based fMRI has been used to study the effects of experimental inflammation on the human brain, but it remains unknown whether intrinsic connectivity in the brain at rest changes during a sickness response. Here, we investigated the effect of experimental inflammation on connectivity between areas relevant for monitoring of bodily states, motivation, and subjective symptoms of sickness. In a double blind randomized controlled trial, 52 healthy volunteers were injected with 0.6 ng/kg LPS (lipopolysaccharide) or placebo, and participated in a resting state fMRI experiment after approximately 2h 45 minutes. Resting state fMRI data were available from 48 participants, of which 28 received LPS and 20 received placebo. Bilateral anterior and bilateral posterior insula sections were used as seed regions and connectivity with bilateral orbitofrontal and cingulate (anterior and middle) cortices was investigated. Back pain, headache and global sickness increased significantly after as compared to before LPS, while a non-significant trend was shown for increased nausea. Compared to placebo, LPS was followed by increased connectivity between left anterior insula and left midcingulate cortex. This connectivity was significantly correlated to increase in back pain after LPS and tended to be related to increased global sickness, but was not related to increased headache or nausea. LPS did not affect the connectivity from other insular seeds. In conclusion, the finding of increased functional connectivity between left anterior insula and middle cingulate cortex suggests a potential neurophysiological mechanism that can be further tested to understand the subjective feeling of malaise and discomfort during a sickness response.
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20.
  • Lindstedt, Fredrik, et al. (författare)
  • Serotonin-1A Receptor Polymorphism (rs6295) Associated with Thermal Pain Perception
  • 2012
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:8
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Serotonin (5-HT) is highly involved in pain regulation and serotonin-1A (5-HT1A) receptors are important in determining central 5-HT tone. Accordingly, variation in the 5-HT1A receptor gene (HTR1A) may contribute to inter-individual differences in human pain sensitivity. The minor G-allele of the HTR1A single nucleotide polymorphism (SNP) rs6295 attenuates firing of serotonergic neurons and reduces postsynaptic expression of the receptor. Experiments in rodents suggest that 5-HT1A-agonism modulates pain in opposite directions at mild compared to high noxious intensities. Based upon this and several other similar observations, we hypothesized that G-carriers would exhibit a relative hypoalgesia at mild thermal stimuli but tend towards hyperalgesia at higher noxious intensities. Methods: Fourty-nine healthy individuals were selectively genotyped for rs6295. Heat-and cold-pain thresholds were assessed along with VAS-ratings of a range of suprathreshold noxious heat intensities (45 degrees C-49 degrees C). Nociceptive-flexion reflex (NFR) thresholds were also assessed. Results: Volunteers did not deviate significantly from Hardy-Weinberg equilibrium. G-carriers were less sensitive to threshold-level thermal pain. This relative hypoalgesia was abolished at suprathreshold noxious intensities where G-carriers instead increased their ratings of heat-pain significantly more than C-homozygotes. No differences with regard to NFR-thresholds emerged. Conclusion/Significance: To the best of our knowledge this is the first study of human pain perception on the basis of variation in HTR1A. The results illustrate the importance of including a range of stimulus intensities in assessments of pain sensitivity. In speculation, we propose that an attenuated serotonergic tone may be related to a 'hypo- to hyperalgesic' response-pattern. The involved mechanisms could be of clinical interest as variation in pain regulation is known to influence the risk of developing pain pathologies. Further investigations are therefore warranted.
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21.
  • Månsson, Kristoffer N. T., et al. (författare)
  • Anterior insula morphology and vulnerability to psychopathology-related symptoms in response to acute inflammation
  • 2022
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 99, s. 9-16
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: The role of inflammation in common psychiatric diseases is now well acknowledged. However, the factors and mechanisms underlying inter-individual variability in the vulnerability to develop psychopathology related symptoms in response to inflammation are not well characterized. Herein, we aimed at investigating morphological brain regions central for interoception and emotion regulation, and if these are associated with acute inflammation-induced sickness and anxiety responses.Methods: Systemic inflammation was induced using an intravenous injection of lipopolysaccharide (LPS) at a dose of 0.6 ng/kg body weight in 28 healthy individuals, while 21 individuals received an injection of saline (placebo). Individuals' gray matter volume was investigated by automated voxel-based morphometry technique on T1-weighted anatomical images derived from magnetic resonance imaging (MRI). Plasma concentrations of TNF alpha and IL-6, sickness symptoms (SicknessQ), and state anxiety (STAI-S) were measured before and after the injection.Results: A stronger sickness response to LPS was significantly associated with a larger anterior insula gray matter volume, independently from increases in cytokine concentrations, age, sex and body mass index (R-2 = 65.6%). Similarly, a greater LPS-induced state anxiety response was related to a larger anterior insula gray matter volume, and also by a stronger increase in plasma TNF-alpha concentrations (R-2 = 40.4%).Discussion: Anterior insula morphology appears central in the sensitivity to develop symptoms of sickness and anxiety in response to inflammation, and could thus be one risk factor in inflammation-related psychopathologies. Because of the limited sample size, the current results need to be replicated.
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22.
  • Olsson, Mats J., et al. (författare)
  • The Scent of Disease : Human Body Odor Contains an Early Chemosensory Cue of Sickness
  • 2014
  • Ingår i: Psychological Science. - : SAGE Publications. - 0956-7976 .- 1467-9280. ; 25:3, s. 817-823
  • Tidskriftsartikel (refereegranskat)abstract
    • Observational studies have suggested that with time, some diseases result in a characteristic odor emanating from different sources on the body of a sick individual. Evolutionarily, however, it would be more advantageous if the innate immune response were detectable by healthy individuals as a first line of defense against infection by various pathogens, to optimize avoidance of contagion. We activated the innate immune system in healthy individuals by injecting them with endotoxin (lipopolysaccharide). Within just a few hours, endotoxin-exposed individuals had a more aversive body odor relative to when they were exposed to a placebo. Moreover, this effect was statistically mediated by the individuals' level of immune activation. This chemosensory detection of the early innate immune response in humans represents the first experimental evidence that disease smells and supports the notion of a "behavioral immune response" that protects healthy individuals from sick ones by altering patterns of interpersonal contact.
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23.
  • Rademacher, Lena, et al. (författare)
  • Editorial: The Different Faces of Sickness
  • 2021
  • Ingår i: Frontiers in Psychiatry. - : Frontiers Media SA. - 1664-0640. ; 12
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Sickness not only includes symptoms that classically define an infection (e.g., fever, nausea, headache), but also comes along with profound neurobehavioral consequences for the infected individual. These include anhedonia, anorexia, pain, lethargy, fatigue, sleepiness, and social withdrawal, and are collectively called “sickness behavior”. Sickness behavior in the infected individual is triggered by mediators of the activated immune system that signal to the brain, thus linking the immunological (inflammatory) response with the psychological (behavioral) response to a pathogen. These inflammatory mediators include cytokines (e.g., interleukins, IL; tumor necrosis factor, TNF) that can be assessed in the circulation in addition to clinical markers of inflammation (e.g., C-reactive protein, CRP). Inflammation and sickness behavior are paralleled by neuroendocrine changes including activation of the autonomic nervous system and the hypothalamus-pituitary-adrenal (HPA) axis, which are both critical for the feedback regulation of the immune response.
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24.
  • Sarlus, Heela, et al. (författare)
  • Allergy influences the inflammatory status of the brain and enhances tau-phosphorylation
  • 2012
  • Ingår i: Journal of Cellular and Molecular Medicine (Print). - : Wiley. - 1582-1838 .- 1582-4934. ; 16:10, s. 2401-2412
  • Tidskriftsartikel (refereegranskat)abstract
    • Despite the existing knowledge regarding the neuropathology of Alzheimer's disease (AD), the cause of sporadic forms of the disease is unknown. It has been suggested that systemic inflammation may have a role, but the exact mechanisms through which inflammatory processes influence the pathogenesis and progress of AD are not obvious. Allergy is a chronic inflammatory disease affecting more than 20% of the Western population, but the effects of allergic conditions on brain functions are largely unknown. The aim of this study was to investigate whether or not chronic peripheral inflammation associated with allergy affects the expression of AD-related proteins and inflammatory markers in the brain. On the basis of previously described models for allergy in mice we developed a model of chronic airway allergy in mouse, with ovalbumin as allergen. The validity of the chronic allergy model was confirmed by a consistent and reproducible eosinophilia in the bronchoalveolar lavage (BAL) fluid of allergic animals. Allergic mice were shown to have increased brain levels of both immunoglobulin (Ig) G and IgE with a widespread distribution. Allergy was also found to increase phosphorylation of tau protein in the brain. The present data support the notion that allergy-dependent chronic peripheral inflammation modifies the brain inflammatory status, and influences phosphorylation of an AD-related protein, indicating that allergy may be yet another factor to be considered for the development and/or progression of neurodegenerative diseases such as AD.
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25.
  • Tamm, Sandra, et al. (författare)
  • Evidence of fatigue, disordered sleep and peripheral inflammation, but not increased brain TSPO expression, in seasonal allergy : A [11C]PBR28 PET study
  • 2018
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 68, s. 146-157
  • Tidskriftsartikel (refereegranskat)abstract
    • Allergy is associated with non-specific symptoms such as fatigue, sleep problems and impaired cognition. One explanation could be that the allergic inflammatory state includes activation of immune cells in the brain, but this hypothesis has not been tested in humans. The aim of the present study was therefore to investigate seasonal changes in the glial cell marker translocator protein (TSPO), and to relate this to peripheral inflammation, fatigue and sleep, in allergy. We examined 18 patients with severe seasonal allergy, and 13 healthy subjects in and out-of pollen season using positron emission tomography (n = 15/13) and the TSPO radioligand [11C]PBR28. In addition, TNF-α, IL-5, IL-6, IL-8 and IFN-γ were measured in peripheral blood, and subjective ratings of fatigue and sleepiness as well as objective and subjective sleep were investigated. No difference in levels of TSPO was seen between patients and healthy subjects, nor in relation to pollen season. However, allergic subjects displayed both increased fatigue, sleepiness and increased percentage of deep sleep, as well as increased levels of IL-5 and TNF-α during pollen season, compared to healthy subjects. Allergic subjects also had shorter total sleep time, regardless of season. In conclusion, allergic subjects are indicated to respond to allergen exposure during pollen season with a clear pattern of behavioral disruption and peripheral inflammatory activation, but not with changes in brain TSPO levels. This underscores a need for development and use of more specific markers to understand brain consequences of peripheral inflammation that will be applicable in human subjects.
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26.
  • Tamm, Sandra, et al. (författare)
  • Objective and Subjective Sleep in Rheumatoid Arthritis and Severe Seasonal Allergy : Preliminary Assessments of the Role of Sickness, Central and Peripheral Inflammation
  • 2021
  • Ingår i: Nature and Science of Sleep. - : Dove Medical Press. - 1179-1608. ; 13, s. 775-789
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Disturbed sleep in inflammatory disorders such as allergy and rheumatoid arthritis (RA) is common and may be directly or indirectly related to disease processes, but has not been well characterized in these patient groups, especially not with objective methods.Aim: The present study aimed to characterize objective and subjective sleep in patients with allergy or RA using sleep diaries, one-channel EEG and actigraphy. It also aimed to investigate if sleep measures were associated with central immune activation, assessed using translocator protein (TSPO) positron emission tomography, as well as cytokine markers of peripheral inflammation and disease-specific symptoms or general symptoms of sickness.Methods: In total, 18 patients with seasonal pollen allergy, 18 patients with RA and 26 healthy controls were included in the study. Allergy patients and matched controls were assessed twice, in and out of pollen season, and RA patients and controls were assessed once. Sleep was recorded for approximately 1 week at each occasion.Results: Patients with allergy had increased levels of slow-wave sleep during pollen season. In contrast, patients with RA had less SWS compared to healthy controls, while no differences were observed in sleep duration or subjective sleep quality. Across groups, neither proinflammatory cytokines, grey matter TSPO levels nor general sickness symptoms were associated with objective or subjective measures of sleep. Rhinitis, but not conjunctivitis, was correlated to worse subjective sleep and more slow wave sleep in allergy. Functional status, but not disease activity, predicted lower subjective sleep in RA.Conclusion: This study tentatively indicates that both patients with allergy and RA display sleep alterations but does not support inflammation as an independent predictor of the sleep disturbance across these patient groups.
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27.
  • Tognetti, Arnaud, et al. (författare)
  • Olfactory Cues of Naturally Occurring Systemic Inflammation : A Pilot Study of Seasonal Allergy 
  • 2023
  • Ingår i: Neuroimmunomodulation. - : S. Karger. - 1021-7401 .- 1423-0216. ; 30:1, s. 338-345
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: In an attempt to avoid contact with infectious individuals, humans likely respond to generalized rather than specific markers of disease. Humans may thus perceive a noninfectious individual as socially less attractive if they look (e.g., have facial discolouration), move (e.g., have a slower walking pace), or sound (e.g., sneeze) sick. This pilot study tested whether humans are averse to the body odour of noninfectious individuals with a low-grade systemic inflammation. Methods: We collected the axillary body odour of individuals with severe seasonal allergy (N = 14) and healthy controls (N = 10) during and outside the allergy season and measured serum levels of two inflammatory cytokines (tumour necrosis factor-α and interleukin-5). Independent participants (N = 67) then sampled and rated these odours on intensity and pleasantness. Results: While individuals with seasonal allergy had nominally more unpleasant and intense body odours during the allergy season, relative to outside the allergy season and to healthy controls, these effects were not significant. When examining immune markers, the change in perceived pleasantness of an individual’s body odour (from out-to-inside pollen season) was significantly related to the change in their interleukin-5 levels but not to tumour necrosis factor-α. Discussion: Our findings tentatively suggest that the human olfactory system could be sensitive to inflammation as present in a noncommunicable condition. Larger replications are required to determine the role of olfaction in the perception of infectious and noninfectious (e.g., chronic diseases) conditions.
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28.
  • Zouikr, Ihssane, et al. (författare)
  • Lifetime Modulation of the Pain System via Neuroimmune and Neuroendocrine interactions
  • 2017
  • Ingår i: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 8
  • Forskningsöversikt (refereegranskat)abstract
    • Chronic pain is a debilitating condition that still is challenging both clinicians and researchers. Despite intense research, it is still not clear why some individuals develop chronic pain while others do not or how to heal this disease. In this review, we argue for a multisystem approach to understand chronic pain. Pain is not only to be viewed simply as a result of aberrant neuronal activity but also as a result of adverse early-life experiences that impact an individual's endocrine, immune, and nervous systems and changes which in turn program the pain system. First, we give an overview of the ontogeny of the central nervous system, endocrine, and immune systems and their windows of vulnerability. Thereafter, we summarize human and animal findings from our laboratories and others that point to an important role of the endocrine and immune systems in modulating pain sensitivity. Taking early-life history into account, together with the past and current immunological and endocrine status of chronic pain patients, is a necessary step to understand chronic pain pathophysiology and assist clinicians in tailoring the best therapeutic approach.
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29.
  • Åström, Jenny, et al. (författare)
  • Evaluating the construct validity and internal consistency of the Sickness Questionnaire in a Swedish sample of adults with longstanding pain
  • 2022
  • Ingår i: Scandinavian Journal of Pain. - : Walter de Gruyter GmbH. - 1877-8860 .- 1877-8879. ; 22:1, s. 88-96
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Low-grade inflammation is a possible contributing factor in the development and persistence of chronic primary pain syndromes. Related to inflammatory activity is sickness behavior, a set of behavioral responses including increased pain sensitivity, fatigue, malaise, fever, loss of appetite, as well as depressive behavior and anhedonia. To capture these behavioral responses and their relation to longstanding pain, psychometrically sound self-report questionnaires are needed. The Sickness Questionnaire (SicknessQ) was developed to assess self-reported sickness behavior based on studies on acute immune activation while maintaining relevance for persistent conditions. The aim of the current study was to evaluate aspects of the validity and reliability of the SicknessQ in a Swedish sample of persons with longstanding pain.Methods: Aspects of construct validity were evaluated by means of performing a confirmatory factor analysis (CFA) (testing structural validity) and by relevant hypothesis testing i.e., that ratings of sickness behavior in combination with other related factors (e.g., depression and anxiety) would be significantly related to ratings of avoidance. Reliability was evaluated by means of analyzing the internal consistency of items.Results: Following the CFA, a non-significant Chi-Square test (chi(2) [32, N=190] = 42.95, p=0.094) indicated perfect model fit. Also, the relative fit indices supported adequate model fit (CFI = 0.978; TLI = 0.969; RMSEA = 0.0430). Sickness behavior (p<0.0001), depression (p<0.05) and pain duration (p<0.05) significantly contributed to the regression model, explaining 45% of the total variance in avoidance. Internal consistency was adequate, as indicated by a Cronbach's alpha value of 0.82 for the entire questionnaire.Conclusions: Results indicate that the SicknessQ has adequate structural validity as well as adequate internal consistency, and is significantly associated with avoidance. The SicknessQ appears to have utility as a self-report questionnaire to assess symptoms of sickness behavior for adults with longstanding pain.
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30.
  • Åström Reitan, Jenny L M, et al. (författare)
  • Associations between sickness behavior, but not inflammatory cytokines, and psychiatric comorbidity in chronic pain
  • 2024
  • Ingår i: Psychoneuroendocrinology. - 0306-4530 .- 1873-3360. ; 167
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: Approximately one in five adults experiences chronic pain, often in co-occurrence with depression, insomnia, anxiety, and lower self-rated health. Elevated levels of cytokines, e.g. tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 8 (IL-8), and interleukin 10 (IL-10), have been identified in patients with chronic pain. Depression, insufficient sleep, poor self-rated health, and pain intensity have also been associated with inflammatory biomarkers. This study aimed to investigate the interrelationships between inflammatory biomarkers and depression, insomnia, anxiety, self-rated health, sickness behavior, and pain intensity in patients with chronic pain.METHODS: Self-report questionnaires and blood samples analyzed for plasma levels of inflammatory biomarkers were collected from 80 adult patients with chronic pain. Associations between inflammatory biomarkers (TNF-α, IL-6, IL-8, IL-10, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR)) and depression, insomnia, anxiety, self-rated health, sickness behavior, and pain intensity, were analyzed using bivariate Spearman rank correlation coefficients and regression analyses.RESULTS: Participants were mainly women (72.5 %), with a mean age of 50.8 years, and a reported mean pain duration of 16.7 years. There were significant correlations between insomnia and CRP (rs =.26, p <.05); sex and ESR (rs =.29, p <.05); age and IL-6 (rs =.29, p <.05) and IL-8 (rs =.30, p <.05); BMI and IL-6 (rs =.50, p <.001), CRP (rs =.63, p <.001) and ESR (rs =.42, p <.001). Ratings of depression were positively and significantly related to ratings of sickness behavior and anxiety (β =.32 and β =.40, respectively), explaining 49 % of the total variance in depression ratings. Insomnia was positively and significantly related to sickness behavior (β =.37) explaining 31 % of the total variance in insomnia ratings. Inflammatory biomarkers, however, did not contribute significantly to the models.CONCLUSIONS: Participants reported high levels of symptoms, yet the associations between these ratings and the inflammatory biomarkers were either absent or weak. Also, despite high levels of self-reported sickness behavior, overall the inflammatory status remained within the normal range. Ratings of sickness behavior contributed more than inflammatory markers in explaining ratings of depression and insomnia. The present results point to the complexity of chronic pain, and the challenges of identifying biomarkers that explain symptomatology.
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