Abstract
BackgroundRecently, 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.ResultsUsing 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-α mRNA of the myocardium were assessed by semi-quantitative RT-PCR. Systemic IL-17, IL-6, and TNF-α 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-α mRNA transcript level and serum IL-6, TNF-α level. The differentiation and proliferation of the Th17 cells were unchanged.ConclusionsOur 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.
Highlights
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
Statistical differences were seen when comparing the survive rate of anti-IL-17 therapy with that of isotype control or PBS groups (P < 0.05), There was no statistical difference of survival rate between isotype control and PBS groups (P> 0.05), and no statistical difference was seen between the IL-17mAb and normal mice (P > 0.05)
IL-17mAb alleviated the severity of Viral myocarditis (VMC) The value of heart weight/body weight (HW/BW), pathological scores of heart sections, integrated optical density (IOD) of IL-17 expression in mice receiving IL17mAb were lower than those of isotype control and PBS mice (P < 0.05), but the pathological scores and IOD of IL-17 expression of IL-17mAb treated mice were a little higher than normal mice (P < 0.05)
Summary
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. Coxsackievirus B3 (CVB3), a member of the Picornaviridae family, is the leading cause of viral myocarditis, which can develop into dilated cardiomyopathy [1,2]. Both the direct viral response and immune-mediated mechanisms have been shown to contribute to the pathogenesis of acute injury and subsequent cardiac remodeling [3,4]. Infection of CVB3 in BALB/c murine model can induce myocarditis with a pathological process resembling human disease, this model has been widely used for studying both the acute
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