Abstract
BackgroundRecently, a new subset of CD4+T helper(Th) cell that predominantly secret cytokine interleukin-9(IL-9) is identified, termed Th9 cell. It has been reported to participate in tissue inflammation and autoimmune responses, and induce disease which differed from Th17 cells. Th17 cells have been shown to play a critical role in viral myocarditis (VMC), but whether Th9 cells are involved in the pathogenesis of VMC remains unclear.ResultsBALB/c mice were intraperitoneally (i.p) injected with coxsackie virus B3(CVB3) for establishing VMC models. Control mice were treated with phosphate-buffered saline i.p. On day 0,7,14,21,28,35,42 after injection, myocardial histopathological changes were evaluated by hematoxylin-eosin staining. Splenic Th17 and Th9 cells subsets were analyzed by flow cytometry. And cardiac IL-17, IL-9 mRNA were measured by semi-quantitative reverse transcription-PCR and nested PCR, respectively. Results showed the levels of Th17 cells and IL-17 mRNA obviously increased in VMC mice on 7 day after infection, peaked on day 28, and highly persisted to at least day 42 (p < 0.05). While the frequencies of Th9 cells and IL-9 mRNA showed no significant difference between VMC and control group throughout the course of the experiment(p > 0.05).ConclusionsIt was differentiated Th17 but not Th9 cells significantly elevated in the development of CVB3-induced VMC. The microenvironment of VMC seemed to contribute to the differentiation and proliferation of Th17 rather than Th9 cells. Our preliminary data implied Th9 cells could not protect against VMC nor promote the disease.
Highlights
A new subset of CD4+T helper(Th) cell that predominantly secret cytokine interleukin-9(IL-9) is identified, termed Th9 cell
Multiple studies had established that intraperitoneal inoculation of BALB/c mice with heart-passaged CVB3 (Nancy strain), can induce inflammatory heart disease which closely resembled human viral myocarditis (VMC)[3], and this model has been widely used for investigating VMC
Previous experiments had indicated the major mechanisms in the pathogenesis of VMC were inflammation and autoimmune responses triggered by the viral infection and mediated by T cells[4,5]
Summary
A new subset of CD4+T helper(Th) cell that predominantly secret cytokine interleukin-9(IL-9) is identified, termed Th9 cell. It has been reported to participate in tissue inflammation and autoimmune responses, and induce disease which differed from Th17 cells. Multiple studies had established that intraperitoneal inoculation of BALB/c mice with heart-passaged CVB3 (Nancy strain), can induce inflammatory heart disease which closely resembled human VMC[3], and this model has been widely used for investigating VMC. Previous experiments had indicated the major mechanisms in the pathogenesis of VMC were inflammation and autoimmune responses triggered by the viral infection and mediated by T cells[4,5]. Besides Th1,Th2 and Treg cells, our previous report and other researches demonstrated Th17 cells which preferentially secret cytokine IL-17 might play an important role in mediating inflammation of VMC[6,7,8,9]. The fundamental mechanisms responsible for VMC are not completely clarified
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