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
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
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DOI：
10.1128/iai.68.9.4968-4971.2000
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发表时间：
2000-09-01
影响因子：
3.1
通讯作者：
Nawa, Y
中科院分区：
文献类型：
--
作者：
Onah, DN;Uchiyama, F;Nawa, Y
用年龄匹配的FCRγ基因敲除(FCRγ(-/-))和野生型(FCR Gamma(+/+))C57BL/6小鼠研究了免疫球蛋白Fc受体(FCR)的γ亚基在肠道线虫黏膜防御中的可能作用。用3000只小白鼠皮下感染文氏圆线虫，在感染后第8天和第13天，通过每日粪卵计数和成虫回收率监测感染程度。用双抗体夹心酶联免疫吸附试验检测小鼠血清中肥大细胞蛋白-1(MMCP-1)的释放，用原位肠壁肥大细胞计数法检测空肠末端肥大细胞(MMC)的反应。FCR-Gamma(-/-)小鼠的卵数(P<；0.01)和成虫数量(P<；0.05)显著高于FCR-Gamma(+/+)小鼠，而肥大细胞增殖率与血清MMCP-1的释放相似。结论：MMCP-1的释放可能是自发的，不依赖于肥大细胞通过FCR-γ信号系统脱颗粒，在排出韦氏沙门氏菌过程中似乎没有作用。FCR-γ(-/-)小鼠排虫的延迟可能与MMC不能脱颗粒和释放除MMCP-1以外的效应分子有关，因为FCR-γ缺失取消了肥大细胞脱颗粒反应。
A possible role for the gamma subunit of immunoglobulin Fc receptors (FcR) in mucosal defenses against intestinal nematode parasites was studied using age-matched FcR gamma-knockout (FcR gamma(-/-)) and wild-type (FcR gamma(+/+)) C57BL/6 mice. Mice were infected subcutaneously with 3,000 infective lan ae of Strongyloides venezuelensis, and the degree of infection was monitored by daily fecal egg counts and adult worm recovery on days 8 and 13 post-infection. Mucosal mast cell (MMC) responses were assayed by in situ intestinal mast cell counts in stained histological sections of the jejunum end by measuring mouse mast cell protease 1 (MMCP-1) release in serum using sandwich enzyme-linked immunosorbent assay, FcR gamma(-/-) mite had significantly higher egg counts (P < 0.01) and numbers of adult worms (P < 0.05) than FcR gamma(+/+) mice, but mastocytosis and serum MMCP-1 release were comparable. It mas concluded that MMCP-1 release may be spontaneous, does not depend on mast cell degranulation via the FcR gamma signaling system, and appears to play no role in the expulsion of S. venezuelensis. The delay in worm expulsion in the FcR gamma(-/-) mice might be related to inability of the MMC to degranulate and release effector molecules other than MMCP-1, since FcR gamma deletion abrogates mast cell degranulative responses.