Abstract

Liver granulomatous inflammation and fibrosis were the primary pathological changes observed during Schistosoma japonicum (S. japonicum) infection. In the present study, the characteristics of IL-9 were investigated in the liver of S. japonicum infection C57BL/6 mice. Immunofluorescence, qRT-PCR, and ELISA results demonstrated that the expression of IL-9 significantly increased after infection (P < 0.01). FACS results indicated that the peak of IL-9+ Th9 cells in the liver mononuclear cells appeared at the early phase of infection (week 5), except that Th9 cells, CD8+ Tc cells, NKT and γδT cells could secrete IL-9 in this model. Although IL-9 neutralization has a limited effect on liver granulomatous inflammation, it could decrease the level of fibrosis-associated factor, PC-III, in the serum of infected mice (P < 0.05). Taken together, our results indicated that IL-9 was an important type of cytokine involved in the progression of S. japonicum infection-induced hepatic damage.

Highlights

  • IL-9 was discovered more than 20 years ago and initially described as a T cell and mast cell growth factor, produced by activated Th2 clones in vitro and during Th2-like T cell responses in vivo[9]

  • S. japonicum infection can result in hepatic granulomatous inflammation and fibrosis

  • The results (Fig. 1C) showed that compared to others the changes of TNF, Il-12, IL-5, and GM-CFS were significant, and the level of these cytokines in serum increased on week 5 after infection, peaked on week 6, and began to decrease

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Summary

Introduction

IL-9 was discovered more than 20 years ago and initially described as a T cell and mast cell growth factor, produced by activated Th2 clones in vitro and during Th2-like T cell responses in vivo[9]. IL-4 signalling promoted Th9 cell differentiation, in part, by suppressing the ability of TGF-β to induce the expression of the T regulatory (TReg) cell-associated transcription factor fork head box P3 (FOXP3)[11]. Except Th9 cells, IL-9 could be produced by mast cells, TC9′ cells, natural killer T (NKT) cells, and other CD4+ T cells, including Th17 cells and Foxp3+ T regulatory (Treg) cells[12]. During murine schistosome mansoni infection, IL-9 expression leads to Th2 cytokine-dominated responses, which leads to death[16]. We observed the characteristics of IL-9 induced by Schistosoma japonicum infection in the liver of C57BL/6 mice

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