European cytokine network最新文献

Interleukin-10 (IL-10) is a pleiotropic cytokine, which has both regulatory and stimulatory effects on different immune cell types. Different studies have reported the importance of IL-10 and Transforming growth factor-beta (TGF-β) in the regulation of B cell class switching the production of immunoglobulin A (IgA); however, the underlying mechanisms remain to be fully elucidated. The objective of this study was to investigate the TGF-β response during B stimulation of human B cells by IL-10. Pan B cells of healthy donors were negatively purified by a magnetic cell separation technique. B cells were cultured with multimeric CD40 ligand (mCD40L) and IL-10 for two and seven days. After harvesting in specific days, TGF-β receptor II and surface IgA expression was determined by flow cytometry, while IgA and TGF-β secretion was assessed by enzyme-linked immunosorbent assay. B cells endogenously expressed TGF-β receptor II and after 48 hours cultivation with mCD40L or mCD40L plus IL-10, both the expression of this receptor and the production of TGF-β were significantly increased. Notably, TGF-β levels following stimulation with mCD40L and IL-10 were higher than those produced by B cells stimulated with mCD40L alone. Furthermore, at day 7 and following IL-10 stimulation, there was a significant rise in the amount of IgA secretion by class-switched plasma cells, which was higher than stimulation with mCD40L alone. Our findings suggest that IL-10 can modulate TGF-β production and TGF-β receptor expression in mCD40-activated human B lymphocytes.

Zika virus (ZIKV) is an emerging arbovirus that causes a mosquito-borne disease. Although infection with ZIKV generally leads to mild disease, its recent emergence in the Americas has been associated with an increase in the development of the Guillain-Barré syndrome in adults, as well as with neurological complications, in particular congenital microcephaly, in new-borns. Over the five past years, through the combined efforts of the scientific community, comprehensive remarkable progress aimed at deciphering the clinical, virological, physiopathological, and immunological features of ZIKV infection. This review highlights some of the most recent advances in our understanding of the role of cytokines and chemokines in ZIKV infection, and discusses potential links to pathogenesis.

Dexmedetomidine (Dex), frequently used as an effective sedative, was reported to play a critical role in the protection of multiple organs. However, its underlying mechanism of a putative protective effect on ischemia/reperfusion (I/R)-induced liver injury is still unclear. A hepatocyte injury model was established by treating WRL-68 cells with oxygen and glucose deprivation/reoxygenation (OGD/R). Enzyme Linked Immunosorbent Assay (ELISA) kits were used to determine the level of inflammatory factors (IL-6, IL-1β, and TNF-α), and oxidative stress indicators (ROS, MDA, GSH-Px, and SOD). MTT assay and flow cytometry analysis were used to determine the influence of Dex on cell viability and cell apoptosis. Expression of nuclear factor erythroid-derived 2- like 2 (Nrf2), HO-1, and apoptosis-related proteins (Bax, Bcl-2, caspase3, and caspase9) were detected by qRT-PCR and western blotting. Dex promoted cell viability and suppressed cell apoptosis in OGD/R-treated WRL-68 cells. Dex reduced TNF-α, IL-6, IL-1β, ROS, and MDA production, whereas it increased that of SOD and GSH-Px in OGD/R-treated WRL-68 cells. Moreover, Nrf2, HO-1, and Bcl-2 expression was upregulated, whereas, in contrast, transcripts for Bax, caspase3, and caspase9 were downregulated following Dex treatment under OGD/R. Knockdown of Nrf2 reversed the Dex effects on cell proliferation, apoptosis, and expression of TNF-α, IL-6, IL-1β, ROS, MDA, SOD, and GSH-Px. Dex protects WRL-68 cells against OGD/R-induced injury by inhibiting inflammation, oxidative stress, and cell apoptosis via the activation of Nrf2/HO-1 signaling pathway, suggesting that Dex may be a potential protector against hepatic injury.

This study mainly to explore the change of serum cytokines in wasp sting patients and the potential correlation between cytokines and acute kidney injury (AKI) due to wasp stings. The levels of IL-2, IL-4, IL-6, IL-10, TNF-α, and IFN-γ in 33 wasp sting and 24 healthy people were measured by flow cytometry, the level of IL-17 was detected by enzyme-linked immunosorbent assay and the laboratory examination including inflammatory indicators, muscle enzyme markers, and renal function were detected by automatic biochemical analyzer, blood analyzer, and urine analyzer. The wasp sting patients were divided into AKI (n = 10) and non-AKI groups (n = 23). The correlation between the levels of serum cytokines and laboratory examination results was analyzed. The levels of IL-2, IL-6, IL-10, IFN-γ, and IL-17 were statistically increased in wasp sting patients compared with the controls (P < 0.05). IL-6, IL-10, and IL-17 levels were markedly increased in the AKI group compared with the non-AKI group (P < 0.05). Moreover, compared with non-AKI group, inflammatory markers and muscle enzyme markers were more abnormal in the AKI group. The positive rate of urinary occult blood in the AKI group was higher than that in the non-AKI group. The levels of IL-2, IL-4, IL-6, IFN-γ, and IL-17 correlated positively with white blood cell counts. The levels of IL-2, IL-4, IL-10, IFN-γ, and IL-17 correlated positively with the levels of serum creatinine. The levels of IL-2, IL-4, IL-10, IL-10, and IFN-γ correlated positively with the levels of C-reactive protein. The levels of IL-10, and IFN-γ correlated positively with urinary occult blood. Conclusion: Elevated levels of cytokines in wasp sting patients might be involved in the development and progression of acute kidney injury.

Guillain-Barré syndrome (GBS) is the most common cause of acute paralysis in the United States. Campylobacter jejuni is a common trigger for GBS, igniting autoimmunity as a result of molecular mimicry between C. jejuni lipooligosaccharide (LOS) and host gangliosides. Evidence also suggests an active role for cell-mediated and innate immunity in pathogenesis of GBS. Infection alone is not enough for GBS to develop, infection with the same strain might yield different outcomes in different patients. C. jejuni strains with low to absent molecular mimicry to self-antigens can cause full-blown GBS with positive autoantibodies. A role for T helper 17 and IL-17 in acute phase of GBS is also identified. Currently, no biological treatment is validated for severe, ventilation-dependent patients with GBS, who might not benefit from either IVIG or plasma exchange therapy. Use of biologic agents in treatment-resistant GBS, especially anti-IL-17 agents, such as secukinumab, ixekizumab, and brodalumab, is to be hoped. This review covers up-to-date knowledge on autoimmune mechanisms responsible in different subtypes of GBS: acute inflammatory demyelinating polyneuropathy and acute motor axonal neuropathy; as well as the experimental autoimmune neuritis (EAN), a commonly used animal model of GBS.

There are a limited number of studies that report the polarization of the immune system toward the production of T helper 1 (Th1), Th2, or Th17-type cytokines in patients with Behçet's disease (BD). Here, we aimed to detect the presence of various cytokines in serum samples of Egyptian BD patients and to determine the correlation between their production levels and clinical manifestations. To that aim, serum levels of IFN-γ, IL-10, IL-6, and IL-17 measured by ELISA were determined in BD patients with active or inactive disease to evaluate their clinical relevance. The results of the present study show significantly elevated levels of IL-17 and IL-6, as well as a reduction in IL-10, and no change in IFN-γ, in sera of BD patients, as compared to the healthy control group. Moreover, IL-6 serum levels were increased in BD patients in active stages of disease and correlated with arthritic manifestations. On the other hand, IL-10 serum levels were significantly decreased in patients with gastrointestinal tract complications. Furthermore, a positive correlation was observed between IL-10 serum levels and ocular manifestations in BD patients, in contrast to those of IL-17, showing no correlation with the different clinical manifestations. Taken together, the magnitude of IL-6 serum levels could be a potential marker for arthritic manifestations and disease activity, whereas those of IFN-γ, IL-10, and IL-17 cannot be considered predictors for different clinical manifestations in patients with BD.

Objective: The aim of our study was to evaluate serum high-sensitivity C-Reactive Protein (hs-CRP), sialic acid (SA), and interleukin-6 (IL-6) levels in pregnancies complicated with preeclampsia (PE) and intrauterine growth restriction (IUGR) and to compare with healthy pregnancies.

Materials and methods: This study was conducted at a tertiary-level maternity hospital with 80 pregnant women. Fasting blood samples were taken from 44 consecutive women with pregnancies complicated by PE (n: 20) and IUGR (n: 24), and 36 were from normal pregnancies. Serum hs-CRP, SA, and IL-6 concentrations were measured in all participants.

Results: Serum mean hs-CRP, SA, and IL-6 levels were higher in the PE and IUGR group when compared with the control group, but this difference was statistically insignificant (P>0.05). No significant correlation was observed between these inflammatory markers (P>0.05).

Conclusion: The serum levels of hs-CRP, SA, and IL-6 were not elevated in pregnancies complicated with PE and IUGR compared with normal pregnancies. Since pregnancy is already a process with inflammation, fluctuations in some markers related to inflammation may be masked by the gestation itself. A local subclinical inflammation may have a role in the pathogenesis of PE and IUGR rather than systemic inflammation.