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Mucosal Defense against Gastrointestinal Nematodes: Responses of Mucosal Mast Cells and Mouse Mast Cell Protease 1 during Primary Strongyloides venezuelensis Infection in FcRγ-Knockout Mice

机译:胃肠道线虫的粘膜防御:FcRγ基因敲除小鼠原发性强直性委内瑞拉感染期间粘膜肥大细胞和小鼠肥大细胞蛋白酶1的反应。

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摘要

A possible role for the γ subunit of immunoglobulin Fc receptors (FcR) in mucosal defenses against intestinal nematode parasites was studied using age-matched FcRγ-knockout (FcRγ−/−) and wild-type (FcRγ+/+) C57BL/6 mice. Mice were infected subcutaneously with 3,000 infective larvae of Strongyloides venezuelensis, and the degree of infection was monitored by daily fecal egg counts and adult worm recovery on days 8 and 13 postinfection. Mucosal mast cell (MMC) responses were assayed by in situ intestinal mast cell counts in stained histological sections of the jejunum and by measuring mouse mast cell protease 1 (MMCP-1) release in serum using sandwich enzyme-linked immunosorbent assay. FcRγ−/− mice had significantly higher egg counts (P < 0.01) and numbers of adult worms (P < 0.05) than FcRγ+/+ mice, but mastocytosis and serum MMCP-1 release were comparable. It was concluded that MMCP-1 release may be spontaneous, does not depend on mast cell degranulation via the FcRγ signaling system, and appears to play no role in the expulsion of S. venezuelensis. The delay in worm expulsion in the FcRγ−/− mice might be related to inability of the MMC to degranulate and release effector molecules other than MMCP-1, since FcRγ deletion abrogates mast cell degranulative responses.
机译:使用年龄匹配的FcRγ敲除(FcRγ-/-)和野生型FcRγ-/-研究了免疫球蛋白Fc受体(FcR)γ亚基在粘膜防御肠道线虫寄生虫中的可能作用sup> + / + )C57BL / 6小鼠。用3000只委内瑞拉氏菌(Strongyloides venezuelensis)感染性幼虫皮下感染小鼠,并在感染后第8天和第13天通过每日粪便卵数和成虫蠕虫恢复监测感染程度。黏膜肥大细胞(MMC)反应通过空肠染色的组织学切片中的原位肠肥大细胞计数以及通过使用夹心酶联免疫吸附测定法测量血清中小鼠肥大细胞蛋白酶1(MMCP-1)的释放来进行测定。 FcRγ-/-小鼠的卵数(P <0.01)和成虫数(P <0.05)明显高于FcRγ + / + 小鼠,但肥大细胞增多和血清MMCP-1版本具有可比性。结论是,MMCP-1释放可能是自发的,不依赖于通过FcRγ信号系统的肥大细胞脱粒,并且似乎在驱逐委内瑞拉葡萄球菌中没有作用。 FcRγ-/-小鼠中蠕虫排出的延迟可能与MMC无法脱粒和释放除MMCP-1以外的效应分子有关,因为FcRγ缺失消除了肥大细胞的脱粒反应。

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