European cytokine network最新文献

The importance of the host inflammatory response, as a central pathological feature of cystic fibrosis, is well recognized. Additionally, hyperglycemia can induce an immune response and consecutively may exacerbate symptoms of this disease. Hence, adherence to a low glycemic index diet, through normalizing blood glucose levels, may reduce inflammation in patients with this disease. This study aimed to compare effects of a low glycemic index/high-fat, high-calorie diet and routine high-fat, high-calorie diet on inflammatory biomarkers in patients with cystic fibrosis. In this randomized clinical trial, 44 children and adolescents with cystic fibrosis were randomly assigned to receive for three months either a high-fat, high-calorie diet (n = 22) or a low glycemic index/high-fat, high-calorie diet (n = 22) with similar calorie and macronutrients composition to the control diet. Patients in first arm were allowed to use all sources of carbohydrates with different glycemic indices, whereas those in another arm consumed carbohydrates from low glycemic index sources. Serum levels of the pro-inflammatory cytokines IL-6, IL-17A, and IFNγ, and the anti-inflammatory cytokine IL-10 were measured at baseline and after the end of the trial. There were significant differences between groups for IL-6 (P = 0.02) and IL-17 (P = 0.01), in favor of the low glycemic diet, but no between-group differences were detected in IL-10 and IFN-γ. Although serum levels of IL-17 were reduced in both the groups as compared with the baseline values, this reduction was only significant in the group assigned to the low glycemic diet (P= 0.007), In addition, IL-6 serum levels decreased and those of IL-10 increased significantly as compared with the baseline values in the low glycemic diet (P= 0.01). It seems that adherence to a low glycemic index/high-fat, high-calorie diet for three months can improve some inflammatory biomarkers in children and adolescents with cystic fibrosis compared with the high-fat, high-calorie diet.

During aging, physiological and physical frailty occur, which is accompanied by a decline in adaptive and innate immunity, termed 'immunosenescence' characterized by marked changes in the composition, function, and competence of the human immune system. Moreover, the capabilities of the immune system to defend the human body against infections, to detect and destruct malignant or autoreactive cells decline, resulting in an increase in the susceptibility to infection, development of cancer, as well as autoimmune disorders. The study of age-related changes in immune function is an important area of investigation. In this review, the function of the immune system during aging, as well as the different ways to rejuvenate the aging immune system, is explored, as medical intervention, balanced nutrition, and a healthy life style will be discussed.

Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is an autoimmune disorder of unknown etiology with dysregulated cytokines levels.

Objectives: The main aim of this study was to assess the clinical correlation between antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, granulomatosis with polyangiitis (GPA) serum levels of the microscopic polyangiitis (MPA), serum levels of the proinflammatory cytokines, interleukin (IL)-32 and interleukin-6.

Methods: Study included 71 patients, 47 with GPA and 24 with MPA. Serum IL-32 and IL-6 concentrations were analyzed in all patients, and compared with levels observed in 10 controls. IL-32 and IL-6 were evaluated using DuoSet and Quantikine HS ELISA, respectively. IL-32 and IL-6 concentrations were correlated with disease-related clinical and laboratory findings.

Results: IL-32 and IL-6 levels were significantly higher in GPA and MPA than in controls, especially IL-32 levels in GPA were elevated. IL-32 concentrations correlated positively with anti-proteinase 3 - ANCA (PR3-ANCA) levels in GPA (P < 0.0001), and with anti-myeloperoxidase ANCA (MPO-ANCA) in MPA (P = 0.049). IL-32 levels correlated positively with disease activity in GPA and MPA (P < 0.0001). GPA patients with pulmonary, cutaneous, and musculoskeletal involvement presented the highest IL-6 serum levels. Cutaneous manifestations correlated positively with IL-6 levels in MPA patients (P = 0.05). ANCA-positive patients with GPA expressed significantly high IL-6 levels (P = 0.036). No significant difference in IL-32 values was observed between ANCA-positive and ANCA-negative patients.

Conclusions: Patients with GPA and MPA present higher serum IL-32 and IL-6 levels than controls. IL-32 levels correlate positively with disease activity.

Tonsils are important lymphoid organs in which B cells and T cells complete their maturation and identify cells that are infected by pathogens. However, the functions of T cells in human tonsils remain unclear, especially the characteristics of polyfunctional CD4⁺ T helper cells. In this study, we used multi-color flow cytometry to analyze the expression or co-expression of effector cytokines in CD4⁺ T cells from tonsillar tissues. We have demonstrated that tonsillar CD4⁺ T cell can express various Th effector cytokines after short-term polyclonal stimulation, and that cytokine-producing CD4⁺ T cells were CD45RO⁺ T cells. In addition, we analyzed the co-expression of two or more kinds of cytokines at the level of a single cell. The results showed that tonsillar CD4⁺ T cells exhibited polyfunctionality by co-expressing two to five kinds of cytokines in the same time. These data furnished a basic theory for further understanding the differentiation of polyfunctional Th cells in human tonsils and their functions in resisting invasive microorganisms.

Introduction: Common Variable Immunodeficiency (CVID) is the most common symptomatic form of primary immunodeficiencies. Current research data show altered B cells, TLRs, and cytokine profile in CVID patients. The aim of this study was to determine levels of IL-1β and IL-6 in CVID patients in response to TLRs stimulation and the association of these cytokines with subtypes of B cells and response to Pneumovax-23 vaccination.

Method: Peripheral blood mononuclear cells of CIVD patients were stimulated with and without TLR2 and TLR4 agonist and specific inhibitors including lipopolysaccharide (LPS), lipoteichoic (LTA), and OxPAPC. The levels of IL-1β and IL-6 were assessed by ELISA in different treatment groups. Finally, association of cytokines levels was assessed among different subtypes of B cells and types of response to Pneumovax-23 vaccine.

Results: Secretion of IL-6 and IL-1β was significantly diminished in CVID patients (p = 0.015 and p = 0.019), but ligand engagement of TLR2 and TLR4 leads to significant increase in IL-6 and IL-1β production. IL-6 was significantly lower in Pneumovax-23 hypo responder patients (p = 0.05) and significant correlations between the concentration of IL-6 and the number of switched memory and CD21^low expressing B cells were found.

Conclusion: Secretion of IL-6 and IL-1β is abolished in CVID patients. However, TLR2 and TLR4 are hyper responsive to stimulation with their cognate ligands resulting in the secretion of higher levels of proinflammatory cytokines. This characteristic of CVID TLRs leads to an improvement of cytokine secretion compared to baseline levels. Also, our novel findings about the association concentrations of serum IL-6 and the frequency of with switched memory and CD21^low expressing B cells as well as the poor response to Pneumovax-23 should be substantiated by the use of a higher sample size in future studies.

This pilot study was designed to compare the levels of interleukin-8 (IL-8), a pro-inflammatory chemokine, in the cerebrospinal fluid (CSF) of patients with Guillain-Barre syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), non-inflammatory polyneuropathy (PNP), and other non-inflammatory neurological diseases (functional syndrome or migraine). The results show elevated CSF IL-8 levels in GBS compared to the other groups (p < 0.05). IL-8 could be considered a potential biomarker to differentiate GBS from CIDP. This distinction could be relevant in terms of therapeutic decisions and functional prognosis.

Background and aims: Chronic hepatic inflammation is an important pathogenic mediator of nonalcoholic fatty liver disease (NAFLD) that contributes to disease severity. It is commonly suggested that autophagy dysfunction may be an underlying cause of nonalcoholic fatty liver disease. However, the exact role of autophagy in lipid metabolism remains controversial. There has been a growing interest in the role of folate supplementation for the treatment and/or prevention of NAFLD. We aimed in this study to investigate the effects of different doses of folate supplementation on several immune markers and autophagy trying to explore the complex role of IL-22 and autophagy in NAFLD.

Methods: Fifty Wistar rats were randomly separated into experimental (n = 40) and control groups (n = 10), which were fed for eight weeks with a high-fat diet (HFD) containing 40% fats or a standard diet, respectively. The experimental group was further subdivided into four subgroups where the first subgroup was left untreated while the other three were treated with different doses of folate (50, 100, and 150 μg/kg of body weight, respectively). At the end of the experimental period, animals from each group were sacrificed for blood and tissue analyses.

Results: NAFLD rats showed decreased IL-22 serum levels and increased LC3B expression as compared to controls. Folate treatment was significantly associated with improvement in disease parameters, reduced presence of the pro-inflammatory cytokines TNF-α and CXCL8 and LC3B expression, and increased IL-22 levels in a dose-dependent manner.

Conclusion: These results highlight the capacity of folate to modulate the production of several pro-inflammatory cytokines and autophagy thereby having a favorable impact disease progression.

Objective: Stage II melanoma patients have high risk for regional and distant metastases and may benefit from novel therapeutic strategies. To clarify the role of NK cells in Stage II melanoma, we characterized the cytotoxic activity of NK cells and the expression of various activating and inhibitory receptors in high-risk cutaneous melanoma patients (Stages IIB and IIC) compared to low-risk patients (Stage IA).

Materials and methods: Native and cytokine-treated peripheral blood mononuclear cells were used for functional and phenotypical analyses.

Results: Compared to Stage IA-B patients, Stage IIB-C patients showed significantly decreased NK cell activity, as well as decreased expression of the activating NKG2D and CD161 receptors, most likely due to increased serum levels of the immunosuppressive cytokine TGF-β1 in these patients. Interestingly, treatment of periperal blood mononuclear cells with IFN-α, IL-2, IL-12 or the combination of IL-12 and IL-18 significantly induced NK cell activity for both groups of melanoma patients. However, only low-risk patients had a significant increase in the expression of the NKG2D receptor after in vitro treatment with IFN-α, as well as an significant increase in the expression of CD161 after treatment with IFN-α or IL-12. Although IL-2 induced the expression of NKG2D in both groups of patients, this increase was significantly lower in high-risk melanoma.

Conclusion: NK cell parameters may be useful as biomarkers of disease progression in localized melanoma patients. Our results further suggest that the use of NK cell-activating cytokines in combination with inhibitors of immunosuppressive factors like TGF-β1 could be a therapeutic option for the treatment of high-risk cutaneous melanoma patients.

Background: Inflammation has a prominent role in cancer development and interleukin (IL)-33 has both inflammatory and anti-inflammatory properties. The aim of this study was to measure IL-33 quantities and genetic alterations in the rs1929992 SNP within IL-33 gene in patients with prostate cancer (PC).

Methods: This investigation was conducted on blood specimens from 150 newly diagnosed PC patients and 150 healthy age-matched controls. Serum IL-33 measurements and genotyping were performed by ELISA and PCR-RFLP, respectively.

Results: Elevated IL-33 quantities were detected in PC patients compared with controls (P < 0.001). The PC patients with Gleason scores 7-10 displayed greater IL-33 quantities than those who had Gleason scores 1-6 (P < 0.001). Significant differences were found between PC stages regarding the IL-33 serum levels (P < 0.001). The frequencies of the genotype GG and allele G in rs1929992 SNP were higher, whereas the frequencies of the genotype AA and allele A were lower in PC patients, as compared with controls (P < 0.05, 0.01, P < 0.002 and P < 0.01, respectively). The genotype GG and allele G of rs1929992 SNP were associated with a greater risk of cancer development (OR: 4.533; P < 0.001, and OR: 1.516; P < 0.01, respectively). The IL-33 levels were not significantly different between the subjects carrier genotypes AA, AG and GG, or alleles A and G in rs1929992 SNP, neither in patients nor in controls.

Conclusion: Higher IL-33 quantities were found in patients with PC, especially in those with greater stages which raises the possiblity that IL-33 may contribute to PC progression. The rs1929992 SNP-related genotype GG and allele G were associated with an increased risk of cancer development.

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