Upon oral infection with Toxoplasma gondii cysts (76 K strain) tachyzoites are released into the intestinal lumen and cross the epithelial barrier causing damage and acute intestinal inflammation in C57BL/6 (B6) mice. Here we investigated the role of microbiota and IL-22 in T.gondii-induced small intestinal inflammation. Oral T.gondii infection in B6 mice causes inflammation with IFNγ and IL-22 production. In IL-22-deficient mice, T.gondii infection augments the Th1 driven inflammation. Deficiency in either IL-22bp, the soluble IL-22 receptor or Reg3γ, an IL-22-dependent antimicrobial lectin/peptide, did not reduce inflammation. Under germ-free conditions, T.gondii-induced inflammation was reduced in correlation with parasite load. But intestinal inflammation is still present in germ-free mice, at low level, in the lamina propria, independently of IL-22 expression. Exacerbated intestinal inflammation driven by absence of IL-22 appears to be independent of IL-22 deficiency associated-dysbiosis as similar inflammation was observed after fecal transplantation of IL-22^-/- or WT microbiota to germ-free-WT mice. Our results suggest cooperation between parasite and intestinal microbiota in small intestine inflammation development and endogenous IL-22 seems to exert a protective role independently of its effect on the microbiota. In conclusion, IL-22 participates in T.gondii induced acute small intestinal inflammation independently of microbiota and Reg3γ.

中文翻译：

---

Interleukin-22 缺乏和微生物群会加剧弓形虫引起的肠道炎症。


弓形虫包囊（76 K 株）口腔感染后，速殖子被释放到肠腔中并穿过上皮屏障，导致 C57BL/6 (B6) 小鼠损伤和急性肠道炎症。在这里，我们研究了微生物群和 IL-22 在弓形虫诱导的小肠炎症中的作用。 B6 小鼠的口腔弓形虫感染会导致炎症并产生 IFNγ 和 IL-22。在 IL-22 缺陷小鼠中，弓形虫感染会加剧 Th1 驱动的炎症。 IL-22bp（可溶性 IL-22 受体）或 Reg3γ（IL-22 依赖性抗菌凝集素/肽）的缺乏并不能减少炎症。在无菌条件下，弓形虫引起的炎症随着寄生虫负载的增加而减少。但肠道炎症仍然存在于无菌小鼠的固有层中，且水平较低，与 IL-22 的表达无关。由 IL-22 缺乏引起的肠道炎症加剧似乎与 IL-22 缺乏相关的生态失调无关，因为在将 IL-22 ^-/-或 WT 微生物群粪便移植到无菌 WT 小鼠后观察到类似的炎症。我们的结果表明寄生虫和肠道微生物群在小肠炎症发展中的合作，并且内源性 IL-22 似乎独立于其对微生物群的影响而发挥保护作用。总之，IL-22 独立于微生物群和 Reg3γ 参与弓形虫诱导的急性小肠炎症。