| 1. |
- Akbarshahi, Hamid, et al.
(författare)
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Early Activation of Pulmonary TGF- β 1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury.
- 2014
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Ingår i: Mediators of Inflammation. - : Hindawi Limited. - 0962-9351 .- 1466-1861. ; 2014:Feb 12
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Tidskriftsartikel (refereegranskat)abstract
- Acute lung injury is caused by many factors including acute pancreatitis. There is no specific therapy directed at underlying pathophysiological mechanisms for acute lung injury. Transforming growth factor- β (TGF- β ) is involved in the resolution of lung injury in later phases of the disease. Some evidence exists demonstrating that TGF- β not only is involved in the late stages, but also contributes to lung injury early on in the progress of the disease. Acute pancreatitis was induced using ductal ligation in mice. TGF- β 1, 2, and 3, T β RII, ALK-5, Smad2, 3, 4, and 7, and P-Smad2 expression in the lungs were analyzed at 9 and 24 h. We demonstrate that TGF- β 1 levels in the lungs of mice with acute pancreatitis increase as early as 9 h after induction. We observed an increased expression of ALK-5 in acute pancreatitis at both 9 and 24 h. Inhibitory Smad7 expression was transiently increased at 9 h in acute pancreatitis, but reduced later at 24 h, with a concomitant increased nuclear translocation of phosphorylated Smad2. Our findings demonstrate activation of TGF- β signaling in the lungs as early as 24 h after acute pancreatitis, suggesting that TGF- β may represent a potential therapeutic candidate in acute pancreatitis-induced acute lung injury.
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| 2. |
- Baars, Erik, et al.
(författare)
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A comparative in vitro study of the effects of separate and combined products of Citrus e fructibus and Cydonia e fructibus on immunological parameters of seasonal allergic rhinitis
- 2012
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Ingår i: Mediators of Inflammation. - : Hindawi Limited. - 0962-9351 .- 1466-1861. ; , s. Art. no. 109829-
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Tidskriftsartikel (refereegranskat)abstract
- This paper examined the effects of the combined product, Citrus e fructibus/Cydonia e fructibus (Citrus/Cydonia; Citrus and Cydonia: each 0.01 g/mL), and separate products of Citrus (0.01 g/mL) and Cydonia (0.01 g/mL) on the immunological pathways involved in seasonal allergic rhinitis (SAR). Peripheral blood mononuclear cells (PBMCs) from five healthy and five grass pollen-allergic donors were isolated and analyzed in vitro after polyclonal and allergen-specific stimulation of T cells in the presence of the three extracts. The analyses demonstrated acceptable cell survival with no signs of toxicity. Citrus mainly had a selective effect on reducing allergen-specific chronic inflammatory (TNF-α; Citrus compared to Cydonia and Citrus/Cydonia: −87.4 ( ? < 0 . 0 0 1 ) and −68.0 ( ? < 0 . 0 5 ), resp.) and Th2 pathway activity (IL-5; Citrus compared to Cydonia: −217.8 ( ? < 0 . 0 1 ); while, both Cydonia and Citrus/Cydonia mainly affected the induction of the allergen-specific Th1 pathway (IFN-γ; Cydonia and Citrus/Cydonia compared to Citrus: 3.8 ( ? < 0 . 0 1 ) and 3.0 ( ? < 0 . 0 1 ), resp.). Citrus and Cydonia demonstrated different working mechanisms in the treatment of SAR and the combination product did not demonstrate larger effects than the separate preparations. Further effectiveness and efficacy studies comparing the effects of the products on SAR in vivo are indicated.
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| 3. |
- Bokarewa, Maria, 1963, et al.
(författare)
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Smoking is associated with reduced leptin and neuropeptide Y levels and higher pain experience in patients with fibromyalgia.
- 2014
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Ingår i: Mediators of inflammation. - : Hindawi Limited. - 1466-1861 .- 0962-9351. ; 2014
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Tidskriftsartikel (refereegranskat)abstract
- Smoking deregulates neuroendocrine responses to pain supporting production of neuropeptide Y (NpY) by direct stimulation of nicotinic receptors or by inhibiting adipokine leptin. Present study addressed the effect of cigarette smoking on adipokines and pain parameters, in 62 women with fibromyalgia (FM) pain syndrome with unknown etiology. Pain was characterized by a visual analogue scale, tender point (TP) counts, pressure pain threshold, and neuroendocrine markers NpY and substance P (sP). Levels of IGF-1, leptin, resistin, visfatin, and adiponectin were measured in blood and cerebrospinal fluid. Current smokers (n = 18) had lower levels of leptin compared to ex-smokers (n = 25, P = 0.002), while the expected NpY increase was absent in FM patients. In smokers, this was transcribed in higher VAS-pain (P = 0.04) and TP count (P = 0.03), lower pain threshold (P = 0.01), since NpY levels were directly related to the pain threshold (rho = 0.414) and inversely related to TP counts (rho = -0.375). This study shows that patients with FM have no increase of NpY levels in response to smoking despite the low levels of leptin. Deregulation of the balance between leptin and neuropeptide Y may be one of the essential mechanisms of chronic pain in FM.
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| 4. |
- Borzecka, Kinga, et al.
(författare)
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CD14 Mediates Binding of High Doses of LPS but Is Dispensable for TNF-alpha Production
- 2013
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Ingår i: Mediators of Inflammation. - : Hindawi Limited. - 0962-9351 .- 1466-1861. ; , s. 824919-
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Tidskriftsartikel (refereegranskat)abstract
- Activation of macrophages with lipopolysaccharide (LPS) involves a sequential engagement of serum LPS-binding protein (LBP), plasma membrane CD14, and TLR4/MD-2 signaling complex. We analyzed participation of CD14 in TNF-alpha production stimulated with 1-1000 ng/mL of smooth or rough LPS (sLPS or rLPS) and in sLPS binding to RAW264 and J744 cells. CD14 was indispensable for TNF-alpha generation induced by a low concentration, 1 ng/mL, of sLPS and rLPS. At higher doses of both LPS forms (100-1000 ng/mL), TNF-alpha release required CD14 to much lower extent. Among the two forms of LPS, rLPS-induced TNF-alpha production was less CD14-dependent and could proceed in the absence of serumas an LBP source. On the other hand, the involvement of CD14 was crucial for the binding of 1000 ng/mL of sLPS judging from an inhibitory effect of the anti-CD14 antibody. The binding of sLPS was also strongly inhibited by dextran sulfate, a competitive ligand of scavenger receptors (SR). In the presence of dextran sulfate, sLPS-induced production of TNF-alpha was upregulated about 1.6-fold. The data indicate that CD14 together with SR participates in the binding of high doses of sLPS. However, CD14 contribution to TNF-alpha production induced by high concentrations of sLPS and rLPS can be limited.
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| 5. |
- Cancemi, Patrizia, et al.
(författare)
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The Role of Matrix Metalloproteinases (MMP-2 and MMP-9) in Ageing and Longevity : Focus on Sicilian Long-Living Individuals (LLIs)
- 2020
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Ingår i: Mediators of Inflammation. - : Hindawi Limited. - 0962-9351 .- 1466-1861. ; 2020
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Tidskriftsartikel (refereegranskat)abstract
- Extracellular matrix metalloproteinases (MMPs) are a group of proteins that activate substrates by enzymatic cleavage and, on the basis of their activities, have been demonstrated to play a role in ageing. Thus, in order to gain insight into the pathophysiology of ageing and to identify new markers of longevity, we analysed the activity levels of MMP-2 and MMP-9 in association with some relevant haematochemical parameters in a Sicilian population, including long-living individuals (LLIs, ≥95 years old). A cohort of 154 healthy subjects (72 men and 82 women) of different ages (age range 20-112) was recruited. The cohort was divided into five subgroups: The first group with subjects less than 40 years old, the second group ranging from 40 to 64 years old, the third group ranging from 65 to 89 years old, the fourth group ranging from 90 to 94 years old, and the fifth group with subjects more than 95 years old. A relationship was observed between LLIs and MMP-2, but not between LLIs and MMP-9. However, in the LLI group, MMP-2 and MMP-9 values were significantly correlated. Furthermore, in LLIs, we found a positive correlation of MMP-2 with the antioxidant catabolite uric acid and a negative correlation with the inflammatory marker C-reactive protein. Finally, in LLIs MMP-9 values correlated directly both with cholesterol and with low-density lipoproteins. On the whole, our data suggest that the observed increase of MMP-2 in LLIs might play a positive role in the attainment of longevity. This is the first study that shows that serum activity of MMP-2 is increased in LLIs as compared to younger subjects. As far as we are concerned, it is difficult to make wide-ranging conclusions/assumptions based on these observations in view of the relatively small sample size of LLIs. However, this is an important starting point. Larger-scale future studies will be required to clarify these findings including the link with other systemic inflammatory and antioxidant markers.
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| 6. |
- Cedervall, Jessica, et al.
(författare)
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Tumor-Induced Local and Systemic Impact on Blood Vessel Function
- 2015
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Ingår i: Mediators of Inflammation. - : Hindawi Limited. - 0962-9351 .- 1466-1861.
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Forskningsöversikt (refereegranskat)abstract
- Endothelial dysfunction plays a role in several processes that contribute to cancer-associated mortality. The vessel wall serves as a barrier for metastatic tumor cells, and the integrity and activation status of the endothelium serves as an important defense mechanism against metastasis. In addition, leukocytes, such as cytotoxic T-cells, have to travel across the vessel wall to enter the tumor tissue where they contribute to killing of cancer cells. Tumor cells can alter the characteristics of the endothelium by recruitment of leukocytes such as neutrophils andmacrophages, which further stimulate inflammation and promote tumorigenesis. Recent findings also suggest that leukocyte-mediated effects on vascular function are not limited to the primary tumor or tissues that represent metastatic sites. Peripheral organs, such as kidney and heart, also display impaired vascular function in tumor-bearing individuals, potentially contributing to organ failure. Here, we discuss how vascular function is altered in malignant tissue and distant organs in individuals with cancer and how leukocytes function as potent mediators of these tumor-induced effects.
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| 7. |
- Çevik Aras, Hülya, 1975, et al.
(författare)
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Monitoring Salivary Levels of Interleukin 1 Beta (IL-1 β) and Vascular Endothelial Growth Factor (VEGF) for Two Years of Orthodontic Treatment: A Prospective Pilot Study
- 2021
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Ingår i: Mediators of Inflammation. - : Hindawi Limited. - 0962-9351 .- 1466-1861. ; 2021
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Tidskriftsartikel (refereegranskat)abstract
- Background and Objective. Vascular endothelial growth factor (VEGF) and interleukin 1 beta (IL-1β) perform functions in orthodontic tooth movement and can be measured in the saliva. This novel approach is aimed at monitoring continuous changes in IL-1β and VEGF levels in saliva during two years of orthodontic treatment. Material and Methods. Nine healthy females (15-20 years of age) with crowding requiring four premolar extractions and fixed appliances in both jaws were included in this prospective pilot study. A total of 134 stimulated and 134 unstimulated saliva samples were collected during two years of treatment: before tooth extractions (baseline) and then every 6-8 weeks at follow-up appointments. All saliva samples were analysed by the enzyme-linked immunosorbent assay. The mean levels of IL-1β and VEGF were calculated according to the different orthodontic treatment stages: alignment, space closure, and finishing. Repeated analysis of variance (ANOVA) measurements were used to compare the means between different treatment stages. The percentage difference in IL-1β and VEGF between the different treatment stages was analysed by Bland-Altman plots. Results. A gradual increase in IL-1β and VEGF was observed at alignment, reaching significance at space closure (p=0.002 and p=0.025, respectively). At finishing, both IL-1β and VEGF declined, however, without reverting to baseline values (p=0.172 and p=0.207, respectively). Bland-Altman analysis showed the agreement between IL-1β and VEGF in terms of a systematic increase, with a higher percentage difference for VEGF. Conclusions. The salivary levels of both IL-1β and VEGF increased following orthodontic treatment and reached their peaks during the treatment stage of space closure. This novel approach provides a hint on how and when to sample saliva during orthodontic treatment to analyse bone remodelling. © 2021 Hülya Çevik-Aras et al.
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| 8. |
- Chen, H, et al.
(författare)
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Folic Acid Supplementation Mitigates Alzheimer's Disease by Reducing Inflammation: A Randomized Controlled Trial
- 2016
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Ingår i: Mediators of inflammation. - : Hindawi Limited. - 1466-1861 .- 0962-9351. ; 2016, s. 5912146-
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Tidskriftsartikel (refereegranskat)abstract
- Background/Aims. Low serum folate levels can alter inflammatory reactions. Both phenomena have been linked to Alzheimer’s disease (AD), but the effect of folic acid on AD itself is unclear. We quantified folate supplementation’s effect on inflammation and cognitive function in patients with AD over the course of 6 months.Methods. Patients newly diagnosed with AD (age > 60 years;n=121; mild to severe; international criteria) and being treated with donepezil were randomly assigned into two groups with (intervention group) or without (control group) supplemental treatment with folic acid (1.25 mg/d) for 6 months. The Mini-Mental State Examination (MMSE) was administered to all patients at baseline and follow-up, and blood samples were taken before and after treatment. We quantified serum folate, amyloid beta (Aβ), interleukin-6 (IL-6), tumor necrosis factorα(TNFα), plasma homocysteine (Hcy), S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), and the mRNA levels of presenilin (PS), IL-6, and TNFαin leukocytes. Data were analyzed using a repeated-measures mixed model.Results. The mean MMSE was slightly increased in the intervention group compared to that in the control group (P<0.05). Posttreatment, plasma SAM and SAM/SAH levels were significantly higher (P<0.05), while Aβ40, PS1-mRNA, and TNFα-mRNA levels were lower in the intervention group than in the control group (P<0.05). The Aβ42/Aβ40ratio was also higher in the intervention group (P<0.05).Conclusions. Folic acid is beneficial in patients with AD. Inflammation may play an important role in the interaction between folic acid and AD. This trial is registered with clinical trial registration numberChiCTR-TRC-13003246.
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| 9. |
- Chu, FN, et al.
(författare)
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Gut Microbiota in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis: Current Applications and Future Perspectives
- 2018
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Ingår i: Mediators of inflammation. - : Hindawi Limited. - 1466-1861 .- 0962-9351. ; 2018, s. 8168717-
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Tidskriftsartikel (refereegranskat)abstract
- The gut environment and gut microbiome dysbiosis have been demonstrated to significantly influence a range of disorders in humans, including obesity, diabetes, rheumatoid arthritis, and multiple sclerosis (MS). MS is an autoimmune disease affecting the central nervous system (CNS). The etiology of MS is not clear, and it should involve both genetic and extrinsic factors. The extrinsic factors responsible for predisposition to MS remain elusive. Recent studies on MS and its animal model, experimental autoimmune encephalomyelitis (EAE), have found that gastrointestinal microbiota may play an important role in the pathogenesis of MS/EAE. Thus, gut microbiome adjustment may be a future direction of treatment in MS. In this review, we discuss the characteristics of the gut microbiota, the connection between the brain and the gut, and the changes in gut microbiota in MS/EAE, and we explore the possibility of applying microbiota therapies in patients with MS.
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| 10. |
- Corona-Meraz, FI, et al.
(författare)
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Inverse Relationship of the CMKLR1 Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance
- 2016
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Ingår i: Mediators of inflammation. - : Hindawi Limited. - 1466-1861 .- 0962-9351. ; 2016, s. 3085390-
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Tidskriftsartikel (refereegranskat)abstract
- Background. In obesity there is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. Chemerin is secreted in white adipose tissue and promotes low-grade inflammatory process, where it expressedCMKLR1receptor. The role of chemerin andCMKLR1in inflammatory process secondary to obesity is not defined yet.Methods. Cross-sectional study with 134 individuals classified as with and without obesity by body mass index (BMI) and IR. Body fat storage measurements and metabolic and inflammatory markers were measured by routine methods. Soluble chemerin and basal levels of insulin by ELISA and relative expression ofCMKLR1were evaluated with qPCR and2-ΔΔCTmethod.Results. Differences (P<0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. BothCMKLR1expression and chemerin levels were increased in obesity without IR. Soluble chemerin levels correlate with adiposity and metabolic markers (r=8.8% to 38.5%),P<0.05.Conclusion. The increment ofCMKLR1expression was associated with insulin production. Increased serum levels of chemerin in obesity were observed, favoring a dysmetabolic response. The results observed in this study suggest that both chemerin andCMKLR1have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.
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