| 1. |
- Bogefors, Jesper, et al.
(författare)
-
LEAP-2, LL-37 and RNase7 in tonsillar tissue: downregulated expression in seasonal allergic rhinitis.
- 2014
-
Ingår i: Pathogens and Disease. - 2049-632X. ; 72:1, s. 55-60
-
Tidskriftsartikel (refereegranskat)abstract
- In the upper airway, the production of antimicrobial peptides (AMPs) protects against bacteria, viruses and fungi. Previous investigations have revealed downregulated expression of AMPs in different manifestations of allergic disease. In this study, we examined the expression of LL-37, RNase7 and LEAP-2 in tonsillar tissue and studied a possible relation to seasonal allergic rhinitis (SAR).
|
|
| 2. |
- Ekman, Anna-Karin, et al.
(författare)
-
Nasal Challenge with LPS Stimulates the Release of Macrophage Inflammatory Protein 1 alpha
- 2009
-
Ingår i: International Archives of Allergy and Immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 149:2, s. 154-160
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Bacterial infections can cause a variety of airway diseases. Toll-like receptors (TLRs) directly respond to the presence of microbes and partake in the innate immune defense. TLR4 is activated by lipopolysaccharide (LPS), and has been detected in sinonasal tissue, epithelial cells and various inflammatory cells. Macrophage inflammatory protein 1 alpha (MIP-1 alpha) is a chemokine released during the inflammatory process. The present study investigated the potential role and regulation of MIP-1 alpha in LPS-induced nasal inflammation. Methods: Thirty-two healthy individuals were intranasally challenged with LPS or vehicle. Nasal lavage was performed, followed by a nasal biopsy. Inflammatory cells were counted, MIP-1 alpha levels analyzed and expression of MIP-1 alpha mRNA in biopsies quantified. Neutrophils isolated from peripheral blood were treated with LPS and effects on MIP1 alpha release, cell survival, and the involved signal pathways, were investigated. Results: LPS challenge caused an increase of MIP-1 alpha in nasal lavage. No corresponding change in mRNA expression was seen in nasal biopsies, suggesting the increase was not due to epithelial synthesis. Neutrophil numbers increased after LPS provocation. Treatment of isolated neutrophils with LPS delayed neutrophil apoptosis and resulted in a time-and concentration-dependent release of MIP-1 alpha, which was reduced by inhibitors of transcription and of nuclear factor (NF)-kappa B, protein kinase C (PKC) and p38 MAPK pathways. Conclusions: Nasal LPS challenge results in release of MIP-1 alpha. The release most likely originates from recruited neutrophils, via NF-kappa B-, PKC-and p38 MAPK-dependent pathways. LPS stimulation delayed neutrophil apop tosis. MIP-1 alpha may constitute an important mediator in neutrophilic airway disease. Copyright (C) 2009 S. Karger AG, Basel
|
|
| 3. |
- Gunnarsdottir, Frida Björk, et al.
(författare)
-
Breast cancer associated CD169(+) macrophages possess broad immunosuppressive functions but enhance antibody secretion by activated B cells
- 2023
-
Ingår i: Frontiers in Immunology. - 1664-3224. ; 14
-
Tidskriftsartikel (refereegranskat)abstract
- CD169(+) resident macrophages in lymph nodes of breast cancer patients are for unknown reasons associated with a beneficial prognosis. This contrasts CD169(+) macrophages present in primary breast tumors (CD169(+) TAMs), that correlate with a worse prognosis. We recently showed that these CD169(+) TAMs were associated with tertiary lymphoid structures (TLSs) and T-regs in breast cancer. Here, we show that CD169(+) TAMs can be monocyte-derived and express a unique mediator profile characterized by type I IFNs, CXCL10, PGE(2) and inhibitory co-receptor expression pattern. The CD169(+) monocyte-derived macrophages (CD169(+) Mo-M) possessed an immunosuppressive function in vitro inhibiting NK, T and B cell proliferation, but enhanced antibody and IL6 secretion in activated B cells. Our findings indicate that CD169(+) Mo-M in the primary breast tumor microenvironment are linked to both immunosuppression and TLS functions, with implications for future targeted Mo-M therapy.
|
|
| 4. |
- Hansson, Lena, 1967-, et al.
(författare)
-
Vitamin D, liver-related biomarkers, and distribution of fat and lean mass in young patients with Fontan circulation
- 2022
-
Ingår i: Cardiology in the Young. - : Cambridge University Press. - 1047-9511 .- 1467-1107. ; 32:6, s. 861-868
-
Tidskriftsartikel (refereegranskat)abstract
- Introduction/aim: Young patients with Fontan circulation may have low serum 25-hydroxyvitamin D levels, an affected liver, and unhealthy body compositions. This study aimed to explore the association between vitamin D intake/levels, liver biomarkers, and body composition in young Fontan patients.Method: We collected prospective data in 2017 to 2018, obtained with food-frequency questionnaires, biochemical analyses of liver biomarkers, and dual-energy X-ray absorptiometry scans in 44 children with Fontan circulation. Body compositions were compared to matched controls (n = 38). Linear regression analyses were used to investigate associations of biomarkers, leg pain, and lean mass on serum levels of 25-hydroxyvitamin D. Biomarkers were converted to z scores and differences were evaluated within the Fontan patients.Results: Our Fontan patients had a daily mean vitamin D intake of 9.9 µg and a mean serum 25-hydroxyvitamin D of 56 nmol/L. These factors were not associated with fat or lean mass, leg pain, or biomarkers of liver status. The Fontan patients had significantly less lean mass, but higher fat mass than controls. Male adolescents with Fontan circulation had a greater mean abdominal fat mass than male controls and higher cholesterol levels than females with Fontan circulation.Conclusion: Vitamin D intake and serum levels were not associated with body composition or liver biomarkers in the Fontan group, but the Fontan group had lower lean mass and higher fat mass than controls. The more pronounced abdominal fat mass in male adolescents with Fontan circulation might increase metabolic risks later in life.
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
- Mansson Kvarnhammar, Anne, et al.
(författare)
-
Diminished levels of nasal S100A7 (psoriasin) in seasonal allergic rhinitis: an effect mediated by Th2 cytokines
- 2012
-
Ingår i: Respiratory Research. - : BioMed Central. - 1465-9921 .- 1465-993X. ; 13:2
-
Tidskriftsartikel (refereegranskat)abstract
- Background: S100A7 is an antimicrobial peptide involved in several inflammatory diseases. The aim of the present study was to explore the expression and regulation of S100A7 in seasonal allergic rhinitis (SAR). less thanbrgreater than less thanbrgreater thanMethods: Nasal lavage (NAL) fluid was obtained from healthy controls before and after lipopolysaccharide (LPS) provocation, from SAR patients before and after allergen challenge, and from SAR patients having completed allergen-specific immunotherapy (ASIT). Nasal biopsies, nasal epithelial cells and blood were acquired from healthy donors. The airway epithelial cell line FaDu was used for in vitro experiments. Real-time RT-PCR and immunohistochemistry were used to determine S100A7 expression in nasal tissue and cells. Release of S100A7 in NAL and culture supernatants was measured by ELISA. The function of recombinant S100A7 was explored in epithelial cells, neutrophils and peripheral blood mononuclear cells (PBMC). less thanbrgreater than less thanbrgreater thanResults: Nasal administration of LPS induced S100A7 release in healthy non-allergic subjects. The level of S100A7 was lower in NAL from SAR patients than from healthy controls, and it was further reduced in the SAR group 6 h post allergen provocation. In contrast, ASIT patients displayed higher levels after completed treatment. S100A7 was expressed in the nasal epithelium and in glands, and it was secreted by cultured epithelial cells. Stimulation with IL-4 and histamine repressed the epithelial S100A7 release. Further, recombinant S100A7 induced activation of neutrophils and PBMC. less thanbrgreater than less thanbrgreater thanConclusions: The present study shows an epithelial expression and excretion of S100A7 in the nose after microbial stimulation. The levels are diminished in rhinitis patients and in the presence of an allergic cytokine milieu, suggesting that the antimicrobial defense is compromised in patients with SAR.
|
|
| 8. |
- Mehmeti-Ajradini, Meliha, et al.
(författare)
-
Human G-MDSCs are neutrophils at distinct maturation stages promoting tumor growth in breast cancer
- 2020
-
Ingår i: Life Science Alliance. - 2575-1077. ; 3:11
-
Tidskriftsartikel (refereegranskat)abstract
- Myeloid-derived suppressor cells (MDSCs) are known to contribute to immune evasion in cancer. However, the function of the human granulocytic (G)-MDSC subset during tumor progression is largely unknown, and there are no established markers for their identification in human tumor specimens. Using gene expression profiling, mass cytometry, and tumor microarrays, we here demonstrate that human G-MDSCs occur as neutrophils at distinct maturation stages, with a disease-specific profile. G-MDSCs derived from patients with metastatic breast cancer and malignant melanoma display a unique immature neutrophil profile, that is more similar to healthy donor neutrophils than to G-MDSCs from sepsis patients. Finally, we show that primary G-MDSCs from metastatic breast cancer patients cotransplanted with breast cancer cells, promote tumor growth, and affect vessel formation, leading to myeloid immune cell exclusion. Our findings reveal a role for human G-MDSC in tumor progression and have clinical implications also for targeted immunotherapy.
|
|
| 9. |
- Mehmeti-Ajradini, Meliha, et al.
(författare)
-
Human G-MDSCs are neutrophils at distinct maturation stages promoting tumor growth in breast cancer
- 2020
-
Ingår i: Life Science Alliance. - : LIFE SCIENCE ALLIANCE LLC. - 2575-1077. ; 3:11
-
Tidskriftsartikel (refereegranskat)abstract
- Myeloid-derived suppressor cells (MDSCs) are known to contribute to immune evasion in cancer. However, the function of the human granulocytic (G)-MDSC subset during tumor progression is largely unknown, and there are no established markers for their identification in human tumor specimens. Using gene expression profiling, mass cytometry, and tumor microarrays, we here demonstrate that human G-MDSCs occur as neutrophils at distinct maturation stages, with a disease-specific profile. G-MDSCs derived from patients with metastatic breast cancer and malignant melanoma display a unique immature neutrophil profile, that is more similar to healthy donor neutrophils than to G-MDSCs from sepsis patients. Finally, we show that primary G-MDSCs from metastatic breast cancer patients co-transplanted with breast cancer cells, promote tumor growth, and affect vessel formation, leading to myeloid immune cell exclusion. Our findings reveal a role for human G-MDSC in tumor progression and have clinical implications also for targeted immunotherapy.
|
|
| 10. |
- Mehmeti, Meliha, et al.
(författare)
-
Wnt5a is a TLR2/4-ligand that induces tolerance in human myeloid cells
- 2019
-
Ingår i: Communications Biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 2
-
Tidskriftsartikel (refereegranskat)abstract
- Innate immune responses are rapid, dynamic and highly regulated to avoid overt reactions. This regulation is executed by innate immune tolerance mechanisms that remain obscure. Wnt5a is a signalling protein mainly involved in developmental processes and cancer. The effect of Wnt5a on inflammatory myeloid cells is controversial. Here, we combine primary cell cultures, in vitro binding studies, mass spectrometry and Drosophila protein modelling to show that Wnt5a is a direct ligand of toll-like receptor (TLR) 2 and 4. The binding promotes a MyD88-non-canonical nuclear factor of kappa B (NFκB) and AP-1 signalling cascade, with contradictory profiles in mouse (pro-inflammatory) and human (anti-inflammatory) myeloid immune cells. These data reveal that the true nature of Wnt5a in inflammatory cells, is to regulate TLR signals, and in human myeloid cells it acts as an endogenous, tolerance-associated molecular pattern (TAMP), inducing IL-10 and innate immune tolerance.
|
|
| 11. |
- Millrud, Camilla Rydberg, et al.
(författare)
-
Docetaxel promotes the generation of anti-tumorigenic human macrophages
- 2018
-
Ingår i: Experimental Cell Research. - : Elsevier BV. - 0014-4827. ; 362:2, s. 525-531
-
Tidskriftsartikel (refereegranskat)abstract
- The taxanes Docetaxel and Paclitaxel are two of the standard chemotherapies for patients with metastatic breast cancer. The functional effect of Docetaxel and Paclitaxel on human innate immune cells of the myeloid lineage is not well established, nor is the effects these agents have on differentiation of monocytes into macrophages and dendritic cells. Therefore, the aim with this project was to determine the effects of Docetaxel and Paclitaxel on primary human monocyte differentiation, activation and function. For this purpose, primary human monocytes were isolated from healthy donors and cultured with or without Docetaxel and Paclitaxel. We found that Docetaxel promoted the differentiation of primary human monocytes into pro-inflammatory macrophages with an M1 phenotype and an ability to present antigens to T cells. Monocytes treated with Docetaxel also displayed an elevated secretion of IL-8 and IL-1β, but did not promote generation of monocytic myeloid-derived suppressor cells. In conclusion, Docetaxel appears to have an immune stimulatory effect that would be beneficial for an anti-tumorigenic type of immune response, whereas Paclitaxel seems to have less effect on myeloid cells.
|
|
| 12. |
- Millrud, Camilla Rydberg, et al.
(författare)
-
Nod-like receptors in head and neck squamous cell carcinoma
- 2013
-
Ingår i: Acta Oto-Laryngologica. - : Informa UK Limited. - 1651-2251 .- 0001-6489. ; 133:12, s. 1333-1344
-
Tidskriftsartikel (refereegranskat)abstract
- Conclusion: The capability of Nod1 to recognize bacteria along with its altered expression and ability to cause an immunological response in head and neck cancer suggest a novel pathway for bacteria to interfere with ongoing cancer inflammation. Objective: Nucleotide oligomerization domain (Nod)-like receptors (NLRs) comprise a recently discovered family of pattern-recognition receptors. In addition to their protective function against infections, accumulating evidence suggests a role for these receptors in various diseases, including cancer. The present study was designed to explore the presence of NLRs in head and neck squamous cell carcinoma, and to determine if these cells have the ability to respond immunologically to ligand stimulation. Methods: The pharyngeal squamous cell carcinoma cell lines Detroit-562 and FaDu were used as a model for head and neck cancer, and compared to healthy primary human nasal epithelial cells. Analyses were performed using immuno-histochemistry, real-time RT-PCR, Luminex Multiplex Immunoassay, ELISA, and flow cytometry. Results: The expression profile of NLRs in head and neck cancer cells differed from that seen in healthy epithelial cells. Further, Nod1 stimulation induced an immunological response in tumor cells that differed from the response in normal epithelial cells, especially regarding the expression of beta-defensin 2, granulocyte monocyte colony stimulating factor (GM-CSF), granulocyte colony stimulating factor (G-CSF), intercellular adhesion molecule-1 (ICAM-1), and cell survival.
|
|
| 13. |
- Millrud, Camilla Rydberg, et al.
(författare)
-
On the origin of myeloid-derived suppressor cells
- 2017
-
Ingår i: Oncotarget. - : Impact Journals, LLC. - 1949-2553. ; 8:2, s. 3649-3665
-
Forskningsöversikt (refereegranskat)abstract
- Myeloid-derived suppressor cells (MDSCs) have a strong immunosuppressive character that allows them to regulate immune responses and hinder overt inflammatory responses. In cancer, this leads to tumor immune evasion and disease progression. MDSCs come in at least two forms: monocytic (Mo-MDSCs) and granulocytic (G-MDSCs). The classical definition of MDSCs as immature myeloid cells blocked from differentiating has been challenged by recent studies suggesting that Mo-MDSCs and G-MDSCs may represent monocytes and granulocytes that have acquired immunosuppressive properties. The molecular mechanism behind their generation and their true origins are now widely debated. In this review we discuss the different proposed mechanisms of the generation of both types of MDSCs, with a special focus on human MDSCs in cancer.
|
|
| 14. |
- Rydberg, Camilla, et al.
(författare)
-
Toll-like receptor agonists induce inflammation and cell death in a model of head and neck squamous cell carcinomas
- 2009
-
Ingår i: Immunology. - : Wiley. - 0019-2805 .- 1365-2567. ; 128:1, s. 600-611
-
Tidskriftsartikel (refereegranskat)abstract
- P>Toll-like receptors (TLRs) are increasingly implicated in the pathogenesis of cancer. The present study describes TLR expression and function in healthy and malignant airway epithelial cells. The squamous cell carcinoma cell line Detroit-562 was compared with the healthy bronchial epithelial cell line NL-20 and primary human nasal epithelial cells (HNECs). TLR2, TLR3 and TLR5 were present in primary head and neck squamous cell carcinomas (HNSCCs). Consistent with this, Detroit-562 expressed TLR2, TLR3 and TLR5, whereas NL-20 expressed mainly TLR3 and HNECs expressed TLR2-5. In Detroit-562, Pam(3)CSK(4), poly(I:C) and flagellin, ligands for TLR2, TLR3 and TLR5, respectively, induced an up-regulation of intercellular adhesion molecule 1 (ICAM-1), an increase in interleukin (IL)-6 and IL-8 secretion and a decrease in cell viability. Additionally, poly(I:C) affected IL-1 beta production and the migratory behaviour of Detroit-562. NL-20 responded with a slight increase in IL-8 secretion upon poly(I:C) stimulation. Poly(I:C) induced a small increase in IL-1 beta, IL-6 and IL-8 production in HNECs, while Pam(3)CSK(4) increased viability. The TLR signalling was transcription-dependent, but the pathways involved differed among TLRs as well as cells. In Detroit-562, TLR2 and TLR5 activation was mediated via c-jun N-terminal kinase (JNK)-, p38-, phosphatidylinositol 3-kinase (PI3K)- and nuclear factor (NF)-kappa B-related pathways, while TLR3 was dependent on NF-kappa B. In NL-20, TLR3 signalled via p38, and in HNECs, NF-kappa B, JNK and extracellular signal-regulated kinase (ERK) appeared to be involved. We found that TLR agonists induced a robust response in HNSCCs, characterized by generation of inflammation and cell death. A similar response was not seen in normal epithelial cells. Thus, the TLR system should be considered an important target in future antitumour immunotherapy.
|
|
| 15. |
- Rydberg Millrud, Camilla
(författare)
-
Pattern-recognition receptors and neutrophils in cancer inflammation
- 2014
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Chronic inflammation, induced by the use of tobacco and alcohol, or caused by infections has long been suggested to constitute a risk factor for head and neck squamous cell carcinoma (HNSCC). The innate immunity is the first line of defense against pathogens, comprising physical and chemical barriers, anti-microbial peptides, pattern-recognition receptors (PRRs) as well as different kinds of cells, including neutrophils. Among the PRRs, Toll-like receptors (TLRs) and Nucleotide oligomerization domain (Nod)-like receptors (NLRs) have gained much attention. They both recognize viruses and bacteria. In addition to their protective role against infections, accumulating evidence suggests a role for these receptors in cancer. Neutrophils are among the first cells to migrate into an inflamed tissue, and their role in various infections is well described. Several studies have demonstrated anti-tumor activities of these cells, but they are also believed to have a tumor-promoting role. Recent data indicate the existence of three distinct neutrophil subsets, CD16dim CD62Lhigh, CD16high CD62Lhigh, and CD16high CD62Ldim cells, with diverse roles in infection, inflammation and cancer. The overall aim with this thesis was to investigate the potential role of PRRs and neutrophils in HNSCC. The thesis demonstrated that the HNSCC cells exhibited high levels of TLR2, TLR3, and TLR5, and a diverse NLR expression. Stimulation of TLR2, TLR3, TLR5, and Nod1 induced a robust inflammatory response and cell death in HNSCC cells that differed from what was seen in corresponding healthy epithelial cells. Following PRR stimulation the cancer cells up-regulated their expression of ICAM-1, and TLR activation increased the secretion of IL-1β, IL-6, and IL-8. In contrast, Nod1 enhanced the production of G-CSF and GM-CSF in HNSCC cells. In addition, the TLRs also affected the survival of the malignant cells. Altogether, this strengthens the suggestion that PRRs might mediate receptor specific tumor effects that can be either anti- or pro-tumorigenic. In the present study of HNSCC, TLRs induced an anti-tumorigenic response, whereas Nod1 activation caused pro-tumorigenic effects. Generally, HNSCC patients had a higher level of leukocytes and specifically more neutrophils in blood than healthy controls. Consequently, the neutrophil/lymphocyte ratio was high in the cancer patients, and a high ratio predicted worse prognosis. The three different neutrophil subsets mentioned above were found in the circulation of patients with HNSCC. The cancer patients exhibited a higher percentage of CD16high CD62Ldim cells than the healthy controls. Among the HNSCC patients, individuals with a high percentage of CD16high CD62Ldim neutrophils had a better outcome. In addition, the CD16high CD62Ldim cells represented the most active neutrophil phenotype. Hence, it might be that these activated neutrophils have anti-tumorigenic properties, and therefore are more favorable for the survival of the HNSCC patients. Altogether this emphasizes the beneficence of having an ongoing process of neutrophil recruitment and activation in patients with HNSCC. Patients with allergic rhinitis (AR) and HNSCC were found to exhibit distinct immunological reactions. The allergic patients exhibited enhanced serum levels of both Th1 and Th2 cytokines. The same increase was also seen in supernatants from their cultured PBMC. In contrast, HNSCC patients had an increase in serum level of cytokines reflecting an innate immune reaction. PMN isolated from these patients showed a generally increased basal activation, and responded strongly to TLR stimulation. Further, tumor biopsies from HNSCC patients displayed a higher Nod2 mRNA expression than nasal biopsies from healthy controls and AR patients outside and during pollen season. All in all, the immune reaction among the allergic patients had an adaptive character with an enhanced T cell activity, whereas the immune reaction of the HNSCC patients was dominated by an innate immune response with suppressed T cells. It is therefore tempting to propose that the enhanced systemic adaptive immune response seen among patients with AR might protect against development of HNSCC. In summary, this thesis demonstrates a receptor specific expression and function of PRRs in HNSCC. It also reveals that the inflammation in HNSCC is dominated by innate immune activities, and that recruitment and activation of neutrophils is important for the survival of these patients. Consequently, the ability to muster a proper inflammatory reaction might be vital for the defense and survival in patient with HNSCC.
|
|
| 16. |
- Rydberg Millrud, Camilla, et al.
(författare)
-
The Activation Pattern of Blood Leukocytes in Head and Neck Squamous Cell Carcinoma Is Correlated to Survival
- 2012
-
Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:12
-
Tidskriftsartikel (refereegranskat)abstract
- Head and neck squamous cell carcinoma (HNSCC) is known to cause substantial immunosuppression. The present study was designed to characterize blood leukocyte activation in HNSCC and to investigate if the individual activation pattern could be related to tumor progress and survival. The leukocyte activation profile of HNSCC patients and healthy controls was assessed with flow cytometry. HNSCC patients displayed increased numbers of monocytes, neutrophils and total leukocytes as well as an enhanced neutrophil/lymphocyte ratio. In addition, patients had a higher percentage of CD69(+), CD71(+) and CD98(+) T cell subsets and NK cells, and a reduced expression of L-selectin in CD14(high)CD16(+) monocytes and neutrophils, when compared to controls. These changes could be correlated to both tumor burden and spread to lymph nodes. Among the cancer patients an increased neutrophil/lymphocyte ratio, a low neutrophil and CD14(high) CD16(+) monocyte activation state and an elevated CD4/CD8 ratio were related to poor survival. In contrast, a high percentage of CD98(+) Th cells appeared to be associated with a better outcome. Taken together, the present data indicate that HNSCC causes activation of blood leukocytes and that the individual activation pattern can be linked to prognosis.
|
|
| 17. |
- Sandberg, Camilla, et al.
(författare)
-
Impaired knee extension muscle strength in adolescents but not in children with Fontan circulation
- 2020
-
Ingår i: Cardiology in the Young. - : Cambridge University Press. - 1047-9511 .- 1467-1107. ; 30:8, s. 1138-1143
-
Tidskriftsartikel (refereegranskat)abstract
- Introduction: Impaired isometric muscle strength was previously reported in adults with Fontan circulation. However, it is unclear if this impairment is present in children and adolescents with Fontan circulation. We investigated isometric muscle strength of the lower limb in patients (6–18 years) with Fontan circulation in comparison with healthy controls.Method: In this cross-sectional study, 43 patients (6–18 years) with Fontan circulation and 43 age- and sex-matched controls were included. Isometric knee extension and plantar flexion muscle strength were assessed using dynamometry (Newton, N). Lean mass of the legs was assessed with dual-energy X-ray absorptiometry. Analyses were performed on group level (n = 43), and for subgroups that included children aged 6–12 years (n = 18) and adolescents aged 13–18 years (n = 25).Results: On group level, the patients with Fontan circulation had impaired isometric knee extension strength in comparison with the controls (p = 0.03). In subgroup analyses, impaired isometric knee extension strength was present in the adolescents (p = 0.009) but not in the children groups. For plantar flexion, there was no difference between patients and controls. There was no difference in lean mass between patients and controls (9.6 ± 4.3 kg vs. 10.8 ± 5.6 kg, p = 0.31). However, the lean mass was highly correlated to isometric knee extension strength (patients r = 0.89, controls r = 0.96, p < 0.001) and isometric plantar flexion strength (patients r = 0.7, controls r = 0.81, p < 0.001).Conclusion: The finding of impaired isometric knee extension muscle strength in adolescents (13–18 years) with Fontan circulation and no corresponding impairment in the children group (6–12 years) could imply that isometric muscle strength gets more impaired with age.
|
|
| 18. |
- Sthen Bergdahl, Magne, et al.
(författare)
-
Calf Muscle Oxygenation is Impaired and May Decline with Age in Young Patients with Total Cavopulmonary Connection
- 2022
-
Ingår i: Pediatric Cardiology. - : Springer. - 0172-0643 .- 1432-1971. ; 43:2, s. 449-456
-
Tidskriftsartikel (refereegranskat)abstract
- Patients palliated with Total Cavopulmonary Connection have a lower muscle mass and a lower exercise capacity. We assessed calf muscle oxidative metabolism during and after heel raise exercise to exhaustion in young patients with TCPC compared to healthy peers. Near-infrared spectroscopy was used for measuring oxygen metabolism in the medial portion of the gastrocnemius muscle. Forty-three patients with TCPC, aged 6–18 years, were compared with 43 age and sex-matched healthy control subjects. Subgroups were formed to include children (6–12 years) and adolescents (13–18 years) to determine if these age groups influenced the results. During exercise, for the patients compared to controls there was a lower increase in deoxygenated hemoglobin (oxygen extraction) (5.13 ± 2.99au vs. 7.75 ± 4.15au, p = 0.001) and a slower rate of change in total hemoglobin (blood volume) (0.004 ± 0.015au vs 0.016 ± 0.01au, p = 0.001). Following exercise, patients exhibited a slower initial increase in tissue oxygenation saturation index (0.144 ± 0.11au vs 0.249 ± 0.226au, p = 0.007) and a longer half-time to maximum hyperemia (23.7 ± 11.4 s vs 16.8 ± 7.5 s, p = 0.001). On the subgroup level, the adolescents differed compared to healthy peers, whereas the children did not. Young patients with TCPC had impaired oxidative metabolism during exercise and required a longer time to recover. In that the differences were seen in the adolescent group and not in the children group may indicate a declining function with age.
|
|
| 19. |
|
|
| 20. |
- Tengroth, Lotta, et al.
(författare)
-
Functional Effects of Toll-Like Receptor (TLR)3, 7, 9, RIG-I and MDA-5 Stimulation in Nasal Epithelial Cells.
- 2014
-
Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:6
-
Tidskriftsartikel (refereegranskat)abstract
- The human nasal epithelium is an important physical barrier, and a part of the innate immune defense that protect against pathogens. The epithelial cells recognize microbial components by pattern-recognition receptors (PRRs), and thereby trigger an immune response. Even though TLR3, TLR7, TLR9, RIG-I and MDA-5 are all known to respond to viral stimulation, their potential role in chronic airway inflammation triggered by local cytokine release remains to be established.
|
|
| 21. |
- Wikner, Anna, et al.
(författare)
-
Lower bone strength in young patients with Fontan circulation compared to controls
- 2024
-
Ingår i: Cardiology in the Young. - : Cambridge University Press. - 1047-9511 .- 1467-1107.
-
Tidskriftsartikel (refereegranskat)abstract
- Objectives: Previous reports indicate bone deficits in patients with Fontan circulation. However, the consequences of these deficits on bone strength and when these changes occur are unclear.Aim: To compare the tibial bone strength-strain index between young patients (6-19 years) with Fontan circulation and age- and sex-matched controls, and to determine strength-strain-index in subgroups of children (6-12 years) and adolescents (13-19 years) versus controls.Method: The tibia was examined with peripheral quantitative CT. Based on the assessed data, bone strength-strain index was calculated in the lateral and anterior-posterior directions.Results: Twenty patients with Fontan and twenty controls (mean age 13.0 ± 4.4 years; 50% females) were examined. Patients had a lower strength-strain index in the lateral direction compared to controls (808.4 ± 416.8mm3 versus 1162.5 ± 552.1mm3, p = 0.043). Subgroup analyses showed no differences regarding strength-strain index in children (6-12 years) with Fontan circulation compared to controls. However, the adolescents (13-19 years) with Fontan circulation had lower strength-strain indexes in both the lateral and anterior-posterior directions compared to controls (1041.4 ± 299.8mm3 versus 1596.4 ± 239.6mm3, p < 0.001, and 771.7 ± 192.4mm3 versus 1084.9 ± 215.0mm3, p = 0.004). When adjusted for height, there were differences between patients (6-19 years) and controls in strength-strain indexes in both the lateral and anterior-posterior directions. In subgroup analyses, the results remained robust.Conclusion: Young patients (6-19 years) with Fontan circulation have a lower strength-strain index in the tibia compared to controls. Subgroup analyses show that this deficit is mainly driven by the differences in adolescents (13-19 years), which might suggest that bone strength decreases with age.
|
|
