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由巴西日圆线虫这种肠道线虫感染所诱导的肺部肉芽肿反应,在肥大细胞缺陷的Ws/Ws大鼠中受到抑制。

Lung granulomatous response induced by infection with the intestinal nematode Nippostrongylus brasiliensis is suppressed in mast cell-deficient Ws/Ws rats.

作者信息

Arizono N, Nishida M, Uchikawa R, Yamada M, Matsuda S, Tegoshi T, Kitamura Y, Sasabe M

机构信息

Department of Medical Zoology, Kyoto Prefectural University of Medicine, Japan.

出版信息

Clin Exp Immunol. 1996 Oct;106(1):55-61. doi: 10.1046/j.1365-2249.1996.d01-803.x.

Abstract

Certain nematode infections induce eosinophil infiltration and granulomatous responses in the lungs. To examine the role of mast cells in the development of lung lesions, normal +/+ and genetically mast cell-deficient Ws/Ws rats were infected with the nematode Nippostrongylus brasiliensis. In +/+ rats, numbers of eosinophils in bronchoalveolar lavage fluid (BALF) increased significantly 3-7 days after infection, and granulomatous responses composed of histiocytes/ macrophages and multinucleate giant cells were triggered in the lungs 3-14 days after infection. Challenge infection, which was carried out on day 28 after primary infection, induced much higher levels of granulomatous response than after primary infection, suggesting that the response is mediated at least in part by an immunological mechanism. In Ws/Ws rats, both the eosinophil percentage in BALF and the size of the granulomas in the lungs were significantly smaller than in +/+ rats after primary as well as after challenge infection. The amount of rat mast cell protease (RMCP) II in +/+ rat BALF was increased 1 day after primary infection and more significantly after challenge infection, suggesting that lung mucosal mast cells were activated more markedly after the challenge infection. In Ws/Ws rats, RMCP II was undetectable throughout the observation period. The time course of nematode migration in the lungs did not differ in +/+ and Ws/Ws rats. These results suggest that mast cell activation might be relevant to eosinophil infiltration and granulomatous response in the lungs, although the responses do not affect lung migration of the nematode.

摘要

某些线虫感染会导致肺部嗜酸性粒细胞浸润和肉芽肿反应。为了研究肥大细胞在肺部病变发展中的作用,将正常的+/+大鼠和基因缺陷型肥大细胞缺乏的Ws/Ws大鼠感染巴西日圆线虫。在+/+大鼠中,感染后3 - 7天支气管肺泡灌洗液(BALF)中的嗜酸性粒细胞数量显著增加,感染后3 - 14天肺部引发了由组织细胞/巨噬细胞和多核巨细胞组成的肉芽肿反应。在初次感染后第28天进行的激发感染诱导的肉芽肿反应水平比初次感染后高得多,这表明该反应至少部分是由免疫机制介导的。在Ws/Ws大鼠中,初次感染以及激发感染后,BALF中的嗜酸性粒细胞百分比和肺部肉芽肿的大小均显著小于+/+大鼠。+/+大鼠BALF中大鼠肥大细胞蛋白酶(RMCP)II的量在初次感染后1天增加,激发感染后增加更显著,这表明激发感染后肺黏膜肥大细胞被更明显地激活。在Ws/Ws大鼠中,在整个观察期内均未检测到RMCP II。线虫在肺部迁移的时间进程在+/+和Ws/Ws大鼠中没有差异。这些结果表明,肥大细胞激活可能与肺部嗜酸性粒细胞浸润和肉芽肿反应有关,尽管这些反应不影响线虫在肺部的迁移。

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