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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mast cells disrupt epithelial barrier function during enteric nematode infection
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Mast cells disrupt epithelial barrier function during enteric nematode infection

机译：肠线虫感染期间肥大细胞破坏上皮屏障功能

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摘要

We have investigated the influence of mast cells on the barrier function of intestinal epithelium during nematode infection. Trichinella spiralis infection induces a strong type 2 cytokine-mediated inflammation, resulting in a critical mucosal mastocytosis that is known to mediate expulsion of the parasites from the intestine. The host response to infection is also characterized by an increase in mucosal leakiness. We show here that intestinal epithelial permeability is markedly elevated during infection, with kinetics that mirror the adaptive immune response to primary and secondary infection. Furthermore, we have identified degradation of the tight junction protein, occludin, thereby providing a mechanism for increased paracellular permeability during helminth infection. We further demonstrate by using anti-c-kit antibody and IL-9 transgenic mice that mast cells are directly responsible for increasing epithelial paracellular permeability and that mice deficient in a mast cell-specific protease fail to increase intestinal permeability and fail to expel their parasite burden. These results provide the mechanism whereby mucosal mast cells mediate parasite expulsion from the intestine. [References: 45]
机译：我们已经研究了线虫感染过程中肥大细胞对肠上皮屏障功能的影响。旋毛虫旋毛虫感染引起强烈的2型细胞因子介导的炎症，导致严重的粘膜肥大细胞增多，已知该介导的介导的肠道寄生虫驱逐。宿主对感染的反应的特征还在于粘膜渗漏的增加。我们在这里显示，肠道上皮通透性在感染过程中明显升高，其动力学反映了对原发和继发感染的适应性免疫反应。此外，我们已经确定紧密连接蛋白occludin的降解，从而提供了在蠕虫感染期间增加细胞旁通透性的机制。通过使用抗c-kit抗体和IL-9转基因小鼠，我们进一步证明了肥大细胞直接负责增加上皮旁细胞通透性，而缺乏肥大细胞特异性蛋白酶的小鼠无法增加肠通透性并且不能驱除它们的寄生虫负担。这些结果提供了粘膜肥大细胞介导寄生虫从肠排出的机制。 [参考：45]

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