Interleukin-33 promotes Th2 immune responses in infected mice with Schistosoma japonicum.

IL-33, a new member of the IL-1 cytokine family, is associated with many infectious diseases. IL-33 not only is crucial for induction of Th2 polarized responses, but also is involved in induction of inflammation as a proinflammatory cytokine. Whether IL-33 leads to beneficial or worsening outcomes depends on the immune mechanism underlying the pathogensis of each disease condition. This study was to elucidate the role of IL-33 in schistosomiasis japonica in a mouse model. Our results demonstrated that serum levels of IL-33 from infected mice with Schistosoma japonicum began to rise at 1 week postinfection (pi) and reached a peak in 7 weeks pi, and then remained a plateau for 2 weeks, after which its level gradually decreased until 12 weeks pi. Compared with the infection control, exogenous IL-33 administration could increase a Th2 polarized immune response (evidenced by higher levels of IL-5, IL-10, and IL-13, along with lower level of IFN-γ) at 6 weeks pi. Meanwhile, this Th2 polarization was associated with higher infection intensity and liver immunopathology in infected mice, whereas injection of anti-IL-33 mAb into infected mice induced adverse effects on these above immune parameters and immunopathology. These data suggest that IL-33 might act as an inducer of Th2 polarization and plays a crucial role in immunopathology in murine schistosomiasis japonica.