tailieunhanh - Báo cáo y học: " Treatment with a neutralizing anti-murine interleukin-17 antibody after the onset of coxsackievirus b3-induced viral myocarditis reduces myocardium inflammation"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Treatment with a neutralizing anti-murine interleukin-17 antibody after the onset of coxsackievirus b3-induced viral myocarditis reduces myocardium inflammation | Fan et al. Virology Journal 2011 8 17 http content 8 1 17 J VIROLOGY JOURNAL RESEARCH Open Access Treatment with a neutralizing anti-murine interleukin-17 antibody after the onset of coxsackievirus b3-induced viral myocarditis reduces myocardium inflammation Yang Fan Wu Weifeng1 2 Yan Yuluan Kong Qing Pang Yu Huang Yanlan Abstract Background Recently some studies indicate that interleukin IL -17 known as a T cell Th17 -derived proinflammatory cytokine is the major mediator of tissue inflammation in inflammatory and autoimmune diseases. Viral myocarditis VMC is a T cell-mediated autoimmune disease but the role for IL-17 in VMC is not well defined. Results Using IL-17 monoclonal antibody IL-17mAb -treated VMC mice we tested the pathogenic role of IL-17 in the development of VMC. VMC mice were treated with monoclonal rat anti-murine IL-17 antibody anti-IL-17 or rat IgG2A isotype control or phosphate-buffered solution 3 days after Coxsackievirus B3 CVB3 injection. Normal mice without any manipulation were taken as normal control. The survival rates of mice were monitored and heart pathology was examined histologically. IL-17 IL-6 and TNF-a mRNA of the myocardium were assessed by semi-quantitative RT-PCR. Systemic IL-17 IL-6 and TNF-a level were measured by enzyme-linked immunosorbent assay and local myocardium IL-17 expression was analyzed using immunohistochemical staining. Flow cytometric analysis was used to evaluate the frequencies of Th17 subsets in CD4 T cells. Results showed that neutralization of IL-17 with anti-IL-17 can ameliorate clinical symptoms defer disease course decrease serum IL-17 level without declining the IL-17 IL-6 and TNF-a mRNA transcript level and serum IL-6 TNF-a level. The differentiation and proliferation of the Th17 cells were unchanged. Conclusions Our data suggest that IL-17 is crucially involved in the pathogenesis of murine VMC IL-17 inhibition might ameliorate the myocardium inflammation after the onset of VMC. .