European cytokine network最新文献

To examine the relationship between metabolic syndrome and serum levels of interleukin (IL)-6 and IL-17, tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP), inflammatory biomarkers involved in nonalcoholic fatty liver disease (NAFLD) pathophysiology, in patients with type 1 diabetes.

Methods: This was a cross-sectional, nested case-control study with 232 patients with type 1 diabetes (116 cases with metabolic syndrome and 116 controls without metabolic syndrome) who were matched for age and gender. A multivariable logistic regression with metabolic syndrome as the dependent variable was performed with inflammatory biomarkers and other parameters involved in NAFLD as independent variables.

Results: Chronic kidney disease (CKD), retinopathy, body mass index (BMI), diabetes duration, alanine aminotransferase (ALT), fatty liver index (FLI), and CPR levels were associated with metabolic syndrome in univariate analysis. However, after adjustments in multivariable analysis, none of the liver-related inflammatory biomarkers persisted associated with metabolic syndrome. CKD, BMI, and ALT were associated with metabolic syndrome and retinopathy showed a tendency for association (p = 0.06).

Conclusion: Although CRP, a nonspecific marker of inflammation, was associated with metabolic syndrome in univariate analysis, this fact did not persist after adjustments. No other inflammatory biomarkers showed an association with metabolic syndrome in type 1 diabetes. The group with metabolic syndrome had a higher frequency of diabetes' complications and markedly increased FLI. FLI probably is more useful in detecting NAFLD than inflammatory biomarkers, but further prospective studies in individuals with type 1 diabetes, with abdominal ultrasound and FLI, are necessary to better support this hypothesis.

Behcet's disease (BD) is a systemic vasculitis, characterized by recurrent oral aphthous, genital ulcers, ocular lesions, and other organ involvement. Interleukin (IL)-27 with its pro- and anti-inflammatory effects might be an important effective cytokine in this disease. The aim of this study was to investigate the association of IL-27 serum concentration and a single-nucleotide polymorphism (SNP) rs153109 (-964 A > G) with the risk and clinical features of the patients with BD. IL-27 Genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and the IL-27 serum levels were measured using enzyme-linked immunosorbent assay (ELISA). It is shown that AG, GG, and AG + GG genotypes, as well as G allele of rs153109, can significantly increase the risk of BD in total and in male individuals. Significantly higher frequencies of AG and GG genotypes and G allele were observed in total and male patients with an active form of BD. AG and GG genotypes were associated with joint (p = 0.046) and vascular (p = 0.02) involvement. The frequency of the G allele was higher in all patients, as well as in female patients with vascular involvement (p = 0.02). Serum cytokine analysis indicated an increased level of IL-27 in BD patients compared to healthy subjects (p = 0.038). Additionally, a higher level of IL-27 was detected in patients carrying the rs153109 GG genotype (p = 0.04) and those with renal (p = 0.009) and skin (p = 0.05) involvement. In conclusion, this study underscores the involvement of IL-27 rs153109 variants and increased serum level in BD susceptibility and pathogenesis.

Both the innate and adaptive arms of the immune system are involved in the development of autoimmune diseases. The main mechanism of disease is due to adaptive immune cells that are active against self-antigens. These cells can cause major damage to body tissues. Innate lymphoid cells (ILCs) are an important type of innate immune cell, whose role has been highlighted in recent years. ILCs are responsible for some of the inflammation in the pathogenesis of autoimmune diseases. In this review, we discuss the role of ILCs in the immune response, as well as their involvement in various autoimmune diseases.

COVID-19 differs substantially between individuals, ranging from mild to severe or even fatal. Heterogeneity in the immune response against SARS-COV-2 likely contributes to this. Therefore, we explored the temporal dynamics of key cellular and soluble mediators of innate and adaptive immune activation in relation to COVID-19 severity and progression. Forty-four patients with a PCR-proven diagnosis of COVID-19 were included. Extensive cellular (leukocytes and T-lymphocyte subsets) and serological immune profiling (cytokines, soluble cell surface molecules, and SARS-CoV-2 antibodies) was performed at hospital admission and every 3-4 days during hospitalization. Measurements and disease outcome were compared between patients with an unfavorable (IC admission and/or death) and favorable (all others) outcome. Patients with an unfavorable outcome had higher leukocyte numbers at baseline, mostly due to increased neutrophils, whereas lymphocyte and monocyte numbers were reduced. CRP, IL-6, CCL2, CXCL10, and GM-CSF levels were higher at baseline in the unfavorable group, whereas IL-7 levels were lower. SARS-CoV-2 antibodies were more frequently absent in the unfavorable group. Longitudinal analysis revealed delayed kinetics of activated CD4 and CD8 T-lymphocyte subsets in the unfavorable group. Furthermore, whereas CRP, IL-6, CXCL10, and GM-CSF declined in the favorable group, these cytokines declined with delayed kinetics, remained increased, or even increased further in the unfavorable group. Our data indicate a state of increased innate immune activation in COVID19-patients with an unfavorable outcome at hospital admission, which remained over time, as compared with patients with a favorable outcome.

Background: Hepatitis C virus (HCV) is the leading cause of chronic liver diseases including hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. We aimed to assess serum levels of interleukin (IL)-22, IL-27 and IL-35 in patients with hepatitis C and healthy controls to investigate their possible relationship with viral genotypes and liver enzyme levels.

Method: A total of 30 newly diagnosed hepatitis C patients with no history of antiviral therapy and 30 healthy individuals participated in this study. Serum levels of IL-22, IL-27 and IL-35 were determined by ELISA in peripheral blood samples from patients prior to and following treament with pan-genotypic direct-acting anti-viral therapy. Serum levels of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP) were measured to determine any possible association between hepatic enzymes and cytokine serum levels concentrations.

Result: The results show elevated serum levels of of IL-35 in HCV-infected patients compared to treated cases and healthy controls, whereas there was no significant difference in IL-22 and IL-27 serum levels among the three groups. Additionally, the cytokine levels were not significantly correlated with certain genotypes and levels of liver enzymes.

Conclusion: Our findings indicate a potential role for IL-35 in chronic HCV infection and therapeutic management of patients with hepatitis C infection.

Type 2 diabetes (T2D) causes profound psychological and physical distress to patients and burdens the health-care system. Although several antidiabetic drugs have been approved, none of them are adequately effective in the long-term management of T2D. Therefore, novel treatment options are needed for disease prevention or delaying disease progression. Bruton's tyrosine kinase (BTK) is a cytoplasmic enzyme that plays a role in B-cell differentiation and proliferation, and therapeutic targeting of BTK offers protection against chronic diseases. In this study, we analyzed BTK expression and its correlation with inflammatory mediators in patients with diabetes and obesity. The levels of BTK were significantly high in visceral adipose tissues of patients (p < 0.01) with diabetes and obesity compared with healthy controls. Additionally, a positive correlation was noted between the expression of BTK and the inflammatory cytokine genes TNF-α, INF-γ, IL-6, and IL-1 (p < 0.01) in adipose tissue. In insulin-resistant HepG2 cells (IR-HepG2), ibrutinib inhibited BTK expression in parallel with inflammatory genes, and increased insulin signaling and activity compared with untreated IR-HepG2 cells. Additionally, ibrutinib-treated IR-HepG2 cells showed increased glucose uptake compared with untreated IR-HepG2 cells. These results provide evidence that BTK inhibition may serve as a novel therapeutic strategy for the treatment of T2D. These findings also uncover the novel role of BTK in diabetes and insulin resistance; however, further in vivo studies are required prior to translating the findings into clinical settings.

Tuberculosis (TB) is one of the leading infectious causes of death worldwide and despite the progress recently made in TB control at a global level, the decline in its incidence is still slow. It is therefore crucial to evaluate the performance of new tools for monitoring of TB treatment. The aim of this study was to evaluate the response to tuberculosis treatment using the QuantiFERON-TB Gold Plus (QFT-Plus) kit. Blood samples of 100 patients with active TB were taken before treatment and after three months, if treatment was successful and sputum culture was negative. Whole blood was incubated in the presence or absence of the TB antigens, TB1 and TB2-specific antigens, and the production of IFN-γ was determined using the QuantiFERON-TB Gold Plus (QFT-Plus) test. The data were analyzed using SPSS 16 software and statistical significance was assessed at a two-tailed P value of 0.05. The median values of IFN-γ released following stimulation with TB1 peptides decreased slightly after treatment (2.5 IU/mL (IQR: 0.9-5.3), compared to the baseline (3.4 IU/mL (IQR: 0.5-6.6)). Also, with respect to the TB1 antigen, 38 out of 45 patients were positive for the QFT test before treatment (84.4%) and 37 cases after treatment (82.2%). On the other hand, the median values of IFN-γ determined with the TB2 test declined marginally after treatment (2.7 IU/mL; IQR: 0.95-5.8), as compared to pretreatment (3.0 IU/mL; IQR: 0.7-8.9). Thirty-nine out of 45 patients (86.7%) before initiation of treatment and 37 cases following a 3-month treatment (82.2%) were had positive values. Moreover, the median values of IFN-γ of TB2 minus TB1 before and after treatment were 0.17 (IQR: 0-1.0) and 0.03 (IQR: 0.0.48), respectively; however, these differences were not significant (p value=0.29). Conclusion: The results of this study show no significant differences between the IFN-γ release in TB patients prior to and after treatment. However, more extensive studies are needed in different populations with higher sample sizes to validate these results.

Coronavirus disease (COVID-19) reached pandemic proportions at the beginning of 2020 and continues to be a worldwide concern. End organ damage and acute respiratory distress syndrome are the leading causes of death in severely or critically ill patients. The elevated cytokine levels in severe patients in comparison with mildly affected patients suggest that cytokine release syndrome (CRS) occurs in the severe form of the disease. In this paper, the significant role of pro-inflammatory cytokines, including IL-1, IL-6, and TNF-alpha, and their mechanism of action in the CRS cascade is explained. Potential therapeutic approaches involving anti-IL-6 and anti-TNF-alpha antibodies to fight COVID-19 and reduce mortality rate in severe cases are also discussed.

Natural cannabinoids may have beneficial effects on various tissues and functions including a positive influence on the immune system and the inflammatory process. The purpose of this study was to investigate the effects of natural cannabinoids on the production of pro-inflammatory cytokines by lipopolysaccharide (LPS)-stimulated whole human blood cells. Levels of the pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were measured before and after exposure of LPS-stimulated whole blood to different concentrations of Cannabidiol (CBD) or a combination of CBD and Tetrahydrocannabinol (THC) extract. LPS stimulated the production of the pro-inflammatory cytokines. Exposure to both CBD and CBD/THC extracts significantly suppressed cytokine production in a dose-dependent manner. Exposure to cannabinoid concentrations of 50 μg/ml or 100 μg/ml resulted in a near-complete inhibition of cytokine production. This study demonstrates that natural cannabinoids significantly suppress pro-inflammatory cytokine production in LPS-stimulated whole blood in a dose-dependent manner. The use of human whole blood, rather than isolated specific cells or tissues, may closely mimic an in vivo sepsis environment. These findings highlight the role that natural cannabinoids may play in suppressing inflammation and call for additional studies of their use as possible novel therapeutic agents for acute and chronic inflammation.

Introduction and aim: Breast cancer (BC) is one of the top three common cancers in women, responsible for nearly one-third of all new cancer diagnoses. Angiogenesis plays a crucial role in BC progression. In this study, we aimed to measure the serum concentrations of eight angiogenic factors in BC patients and healthy controls and to assess their correlation with clinicopathological variables.

Methods: In a case-control study, 62 pathologically confirmed BC patients as well as 54 age-matched controls were recruited. A bead-based immunoassay was used to measure serum levels of VEGF-A, ANG-2, PDGF-AA, PDGF-BB, EGF, TGF-α, HGF, and bFGF.

Results: We observed a significant elevation in serum levels of VEGF-A, EGF, and PDGF-AA in BC patients compared with the controls (P < 0.05). Patients with grade III had higher ANG-2 levels compared with those with grades I (P = 0.007) and II of the disease (P = 0.003). In addition, estrogen-positive and progesterone-positive BC patients had higher levels of TGF-α (P < 0.05).

Conclusion: The significant elevation of VEGF-A, EGF, and PDGF-AA serum levels in BC patients suggests these cytokines might have diagnostic value as potential biomarkers in BC. Further large-scale studies are needed to generalize these results to all BC patients.