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长爪沙鼠(Meriones unguiculatus)对委内瑞拉类圆线虫再感染的黏膜免疫缺陷和全身免疫正常。

Defective mucosal immunity and normal systemic immunity of Mongolian gerbils, Meriones unguiculatus, to reinfection with Strongyloides venezuelensis.

作者信息

Khan A I, Horii Y, Nawa Y

机构信息

Department of Parasitology, Miyazaki Medical College, Japan.

出版信息

Parasite Immunol. 1993 Oct;15(10):565-71. doi: 10.1111/pim.1993.15.10.565.

Abstract

The systemic and local protective activity of Mongolian gerbils was examined after re-infection with Strongyloides venezuelensis. Mongolian gerbils were unable to expel S. venezuelensis adult worms from the intestine for over ten weeks after a primary infection. Therefore, immune animals were prepared by treating with mebendazole four weeks after a primary infection and then they were challenged by different maturation stages of the parasite; subcutaneous inoculation with the infective larvae (L3) obtained by faecal culture, oral administration of L3 obtained from the lungs of rats three days after a primary infection, or oral implantation of adult worms obtained from the intestines of rats seven days after a primary infection. The results show that, although immune animals were highly resistant against challenge infection by subcutaneous inoculation with cultured L3, they were unable to expel orally administered lung-recovered L3 nor orally implanted adult worms. Although potentiated mastocytosis was induced by challenge infections with lung-recovered L3 and adult worms, all mast cells were formalin-resistant, heparin-containing cells and never seen in the epithelial layer. In spite of the defective protective capacity at the intestinal mucosa, circulating antibody production specific to S. venezuelensis adult as well as L3 antigen was positive. Therefore, the inability of Mongolian gerbils to expel S. venezuelensis adult worms from the intestine seems to be due to the defects of effector/regulator cells, presumably mast cells, but not due to immune unresponsiveness to parasite antigen.

摘要

在用委内瑞拉类圆线虫再次感染后,检测了蒙古沙鼠的全身和局部保护活性。初次感染后,蒙古沙鼠在十多周内无法从肠道排出委内瑞拉类圆线虫成虫。因此,在初次感染四周后用甲苯达唑进行处理来制备免疫动物,然后用寄生虫的不同成熟阶段对它们进行攻击;通过粪便培养获得的感染性幼虫(L3)皮下接种、初次感染三天后从大鼠肺部获得的L3口服给药,或初次感染七天后从大鼠肠道获得的成虫口服植入。结果表明,尽管免疫动物对通过皮下接种培养的L3进行的攻击感染具有高度抗性,但它们无法排出口服给药的肺部回收的L3或口服植入的成虫。尽管肺部回收的L3和成虫的攻击感染诱导了肥大细胞增多,但所有肥大细胞都是耐福尔马林、含肝素的细胞,从未在上皮层中见到。尽管肠道黏膜的保护能力存在缺陷,但针对委内瑞拉类圆线虫成虫以及L3抗原的循环抗体产生呈阳性。因此,蒙古沙鼠无法从肠道排出委内瑞拉类圆线虫成虫似乎是由于效应/调节细胞(可能是肥大细胞)的缺陷,而不是由于对寄生虫抗原的免疫无反应性。

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