The inflammasome is a key line of immune defense against invading infectious pathogens. However, knowledge of the role of nod-like receptor pyrin domain containing 3 (NLRP3) in Trichinella spiralis infection which characteristically induces T-helper 2 (Th2) immune responses is sparse. In this study, we investigated the role of NLRP3 in the protection against T. spiralis infection through the Th2 immune response. We show that NLRP3 expression in CD4⁺ T cells was significantly increased at 7 days post-infection of T. spiralis. Compared to wild-type (WT) CD4⁺ T cells, the expression of IL-4 mRNA was reduced in NLRP3^−/− CD4⁺ T cells, however, the expression of IFN-γ mRNA was comparable between the two groups. Consistently, ELISA and flow cytometry analysis showed that NLRP3^−/− CD4⁺ T cells secreted lower levels of IL-4 than CD4⁺ T cells from WT mice, whilst the levels of IFN-γ secreted by NLRP3^−/− CD4⁺ T cells were of similar levels to those secreted by WT CD4⁺ T cells. In addition, we observed a significant reduction of IL-4 and IL-13 by ELISA in NLRP3 ^−/− mice at 1, 2 and 4 weeks post-infection. Furthermore, we found that adult worm survival was substantially prolonged and muscle larvae burden was significantly increased in NLRP3 ^−/− mice. We further show that NLRP3 promotes the host defense against T. spiralis through its participation in the differentiation of Th2 cells. These findings provide novel insights into parasite expulsion and highlight the importance of NLRP3 in the host defense against T. spiralis.

炎性体是抵抗入侵传染性病原体的免疫防御的关键线。然而，关于含有 3 (NLRP3) 的 nod 样受体 pyrin 结构域在特征性诱导 T 辅助 2 (Th2) 免疫反应的旋毛虫感染中的作用的知识很少。在这项研究中，我们通过 Th2 免疫反应研究了 NLRP3 在防止螺旋线虫感染中的作用。我们显示在感染 T.spiralis 后 7 天，CD4 ^{+ T 细胞中的}NLRP3表达显着增加。与野生型 (WT) CD4 ^{+ T 细胞相比，NLRP3 -/-} CD4 ⁺ T 细胞中 IL-4 mRNA 的表达降低然而，T 细胞中 IFN-γ mRNA 的表达在两组之间具有可比性。一致地，ELISA和流式细胞术分析显示，来自WT小鼠的NLRP3 ^-/- CD4 ⁺ T细胞分泌的IL-4水平低于CD4 ^{+ T细胞，而NLRP3 -/-} CD4 ⁺ T细胞分泌的IFN-γ水平与WT CD4 ⁺ T细胞分泌的水平相似。此外，我们通过 ELISA 观察到 NLRP3 ^-/-小鼠在感染后 1、2 和 4 周时 IL-4 和 IL-13 显着减少。此外，我们发现 NLRP3 中成虫的存活率显着延长，肌肉幼虫负担显着增加^-/-老鼠。我们进一步表明， NLRP3通过参与 Th2 细胞的分化来促进宿主对 T.spiralis 的防御。这些发现为寄生虫驱除提供了新的见解，并强调了 NLRP3 在宿主防御 T.spiralis 中的重要性。