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感染曼氏血吸虫的大鼠会出现肝脏募集肥大细胞的情况,但感染的小鼠则不会。

Hepatic recruitment of mast cells occurs in rats but not mice infected with Schistosoma mansoni.

作者信息

Miller H R, Newlands G F, McKellar A, Inglis L, Coulson P S, Wilson R A

机构信息

Department of Veterinary Clinical Studies, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Scotland, UK.

出版信息

Parasite Immunol. 1994 Mar;16(3):145-55. doi: 10.1111/j.1365-3024.1994.tb00334.x.

DOI:10.1111/j.1365-3024.1994.tb00334.x
PMID:8208587
Abstract

The pathogenesis of infection with Schistosoma mansoni in rats is distinct from that in mice. Rats are non-permissive hosts and infection is terminated in the liver before egg laying commences whereas the parasites completes its life cycle in mice. Comparison of the mast cell responses in the two species reveals that a pronounced hepatic mastocytosis occurs in the rat and this is concomitant with the demise of the parasite. The majority of recruited hepatic mast cells contain the highly soluble granule chymase, rat mast cell protease-II, which is released systemically into blood during the period of parasite elimination. In contrast, very few mast cells are found in livers of parasitized mice and none contain the soluble granule chymase mouse mast cell protease-1. However, during egg deposition in the gut, an intraepithelial mastocytosis occurs in parasitized mice. These intraepithelial cells are typical mucosal mast cells as determined by their content of mouse mast cell protease-1. Recruitment of mucosal mast cells occurs in the intestinal lamina propria of infected rats soon after the parasites migrate to the liver. These findings suggest that mast cells of the mucosal phenotype are involved in the pathogenesis of the hepatic response to infection in the rat but that, in the mouse, mucosal mastocytosis is associated with intestinal sensitization by egg antigens.

摘要

曼氏血吸虫感染大鼠的发病机制与感染小鼠的不同。大鼠是非适宜宿主,感染在肝脏中终止,此时尚未开始产卵,而寄生虫在小鼠体内可完成其生命周期。对这两个物种肥大细胞反应的比较显示,大鼠肝脏出现明显的肥大细胞增多症,这与寄生虫的死亡同时发生。大多数被招募到肝脏的肥大细胞含有高度可溶性颗粒糜蛋白酶,即大鼠肥大细胞蛋白酶-II,在寄生虫清除期间,它会被全身释放到血液中。相比之下,在感染寄生虫的小鼠肝脏中发现的肥大细胞很少,且没有一个含有可溶性颗粒糜蛋白酶小鼠肥大细胞蛋白酶-1。然而,在肠道虫卵沉积期间,感染寄生虫的小鼠会出现上皮内肥大细胞增多症。根据其小鼠肥大细胞蛋白酶-1的含量确定,这些上皮内细胞是典型的黏膜肥大细胞。在寄生虫迁移到肝脏后不久,感染大鼠的肠道固有层就会出现黏膜肥大细胞的募集。这些发现表明,黏膜表型的肥大细胞参与了大鼠肝脏对感染反应的发病机制,但在小鼠中,黏膜肥大细胞增多症与虫卵抗原引起的肠道致敏有关。

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