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Polarizing the T helper 17 response in Citrobacter rodentium infection via expression of resistin-like molecule α

机译:通过抵抗素样分子α的表达来极化啮齿动物柠檬酸杆菌感染中的T辅助17反应。

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摘要

Citrobacter rodentium infection is a murine model of pathogenic Escherichia coli infection that allows investigation of the cellular and molecular mechanisms involved in host-protective immunity and bacterial-induced intestinal inflammation. We recently demonstrated that following C. rodentium infection, the absence of Resistin-Like Molecule (RELM) α resulted in attenuated Th17 cell responses and reduced intestinal inflammation with minimal effects on bacterial clearance. In this addendum, we investigated the cytokine modulatory effects of RELMα and RELMα expression in the intestinal mucosa following C. rodentium infection. We show that in addition to promoting Th17 cytokine responses, RELMα inhibits Th2 cytokine expression and Th2-cytokine effector macrophage responses in the C. rodentium-infected colons. Second, utilizing reporter C. rodentium, we examined RELMα expression and macrophage recruitment at the host pathogen interface. We observed infection-induced macrophage infiltration and RELMα expression by intestinal epithelial cells. The influence of infection-induced RELMα on macrophage recruitment in the intestine is discussed.
机译:啮齿动物柠檬酸杆菌感染是一种致病性大肠杆菌感染的小鼠模型,可用于研究与宿主保护性免疫和细菌引起的肠道炎症有关的细胞和分子机制。我们最近证明,在感染了啮齿类杆菌之后,缺乏抵抗素样分子(RELM)α导致Th17细胞反应减弱,肠道炎症减少,对细菌清除的影响最小。在本附录中,我们研究了啮齿类念珠菌感染后肠道粘膜中RELMα和RELMα表达的细胞因子调节作用。我们显示,除了促进Th17细胞因子反应,RELMα还可以抑制C.rodentium感染结肠中Th2细胞因子表达和Th2-细胞因子效应巨噬细胞反应。其次,利用报告子啮齿类动物,我们检查了宿主病原体界面的RELMα表达和巨噬细胞募集。我们观察到肠上皮细胞感染引起的巨噬细胞浸润和RELMα表达。讨论了感染诱导的RELMα对肠道巨噬细胞募集的影响。

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