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在免疫功能正常的小鼠感染和再次感染隐孢子虫鼠时,胃黏膜中保护性细胞介导免疫应答的激活。

Activation of protective cell-mediated immune response in gastric mucosa during Cryptosporidium muris infection and re-infection in immunocompetent mice.

机构信息

Faculty of Science, University of South Bohemia in Ceské Budejovice, Branisovská 31, 370 05, Ceské Budejovice, Czech Republic.

出版信息

Parasitol Res. 2010 Apr;106(5):1159-66. doi: 10.1007/s00436-010-1785-2. Epub 2010 Feb 13.

DOI:10.1007/s00436-010-1785-2
PMID:20155366
Abstract

Gastric cryptosporidia only inhabit the glandular part of the stomach of all age categories of their hosts and can cause chronic life-long infections independent of a host's immune status. The immune response in the stomach mucosa during the primary infection and re-infection with Cryptosporidium muris (TS03 and CB03) in immunocompetent BALB/c mice was characterized using flow cytometry analysis and measurement of IFN-gamma and IL10 by enzyme-linked immunosorbent assays (ELISA). Significantly, elevated migration of T lymphocytes (more than 1,000-fold), especially CD8+ T lymphocytes, to the stomach mucosa occurred during primary infection and persisted for more than 2 months after its resolution. The ex vivo cultures of splenocytes revealed very low levels of IFN-gamma production during the course of the primary infection (0.5 ng/ml), whereas in the following re-exposure to the parasites, the concentration of IFN-gamma rapidly increased 22-fold. Although the two parasite strains that were tested were genetically distinct, they yielded similar results in the induction of cellular immune responses, suggesting that these patterns are not unique to a single parasite strain. These results imply that the CD8+ T lymphocytes are involved in the immune response to gastric cryptosporidiosis and could play an important role in the elimination of C. muris infection in mice.

摘要

胃隐孢子虫仅栖息于其宿主所有年龄段的腺体部分,并且可以在不依赖宿主免疫状态的情况下引起慢性终身感染。使用流式细胞术分析和酶联免疫吸附试验(ELISA)测量 IFN-γ和 IL10,来描述初次感染和再次感染免疫功能正常的 BALB/c 小鼠时胃黏膜中的免疫反应。值得注意的是,在初次感染期间,T 淋巴细胞(超过 1000 倍),尤其是 CD8+T 淋巴细胞向胃黏膜的迁移明显增加,并在其解决后持续超过 2 个月。脾细胞的离体培养显示,在初次感染过程中 IFN-γ的产生水平非常低(0.5ng/ml),而在随后再次暴露于寄生虫时,IFN-γ的浓度迅速增加 22 倍。尽管测试的两种寄生虫株在遗传上是不同的,但它们在诱导细胞免疫反应方面产生了相似的结果,这表明这些模式不是特定于单一寄生虫株的。这些结果表明,CD8+T 淋巴细胞参与了对胃隐孢子虫病的免疫反应,并可能在消除小鼠中的 C. muris 感染中发挥重要作用。

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