Infection with a helminth parasite prevents experimental colitis via a macrophage-mediated mechanism
Infection with a helminth parasite prevents experimental colitis via a macrophage-mediated mechanism
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DOI：
10.4049/jimmunol.178.7.4557
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发表时间：
2007-04-01
影响因子：
4.4
通讯作者：
Fallon, Padraic G.
中科院分区：
文献类型：
--
作者：
Smith, Philip;Mangan, Niamh E.;Fallon, Padraic G.
一系列寄生蠕虫刺激Th 2或调节细胞偏向性反应的倾向已被提出，以降低实验性炎症性肠病的严重程度。我们检查了曼氏血吸虫（一种吸虫寄生虫）的感染是否改变了小鼠对葡聚糖硫酸钠（DSS）诱导的结肠炎的易感性。感染寄生蠕虫的小鼠对DSS诱导的结肠炎是难治的。产蛋的寄生虫感染或注射鸡蛋并没有使小鼠对DSS诱导的结肠炎产生抗性。血吸虫感染通过依赖于巨噬细胞的新机制预防结肠炎，而不是通过简单的调节Th 2应答，或通过诱导调节性CD 4（+）或CD 25（+）细胞，IL-10或TGF-β。感染小鼠的结肠固有层中有明显的巨噬细胞（F4/80（+）CD 11b（+）CD 11 c（-））浸润，并且对DSS诱导的结肠炎的保护被证明是巨噬细胞依赖性的。结肠炎的耐药性不是由于交替激活的巨噬细胞。转移从蠕虫感染的小鼠中分离的结肠固有层F4/80（+）巨噬细胞在用DSS处理的受体小鼠中诱导了对结肠炎的显著保护。因此，我们提出了一种新的机制，寄生虫通过一种新的结肠浸润巨噬细胞群体抑制DSS诱导的结肠炎。
The propensity of a range of parasitic helminths to stimulate a Th2 or regulatory cell-biased response has been proposed to reduce the severity of experimental inflammatory bowel disease. We examined whether infection with Schistosoma mansoni, a trematode parasite, altered the susceptibility of mice to colitis induced by dextran sodium sulfate (DSS). Mice infected with schistosome worms were refractory to DSS-induced colitis. Egg-laying schistosome infections or injection of eggs did not render mice resistant to colitis induced by DSS. Schistosome worm infections prevent colitis by a novel mechanism dependent on macrophages, and not by simple modulation of Th2 responses, or via induction of regulatory CD4(+) or CD25(+) cells, IL-10, or TGF-beta. Infected mice had marked infiltration of macrophages (F4/80(+)CD11b(+)CD11c(-)) into the colon lamina propria and protection from DSS-induced colitis was shown to be macrophage dependent. Resistance from colitis was not due to alternatively activated macrophages. Transfer of colon lamina propria F4/80(+) macrophages isolated from worm-infected mice induced significant protection from colitis in recipient mice treated with DSS. Therefore, we propose a new mechanism whereby a parasitic worm suppresses DSS-induced colitis via a novel colon-infiltrating macrophage population.