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首页> 外文期刊>Infection and immunity >Soluble invasion plasmid antigen C (IpaC) from Shigella flexneri elicits epithelial cell responses related to pathogen invasion.
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Soluble invasion plasmid antigen C (IpaC) from Shigella flexneri elicits epithelial cell responses related to pathogen invasion.

机译：来自弗氏志贺氏菌的可溶性入侵质粒抗原C（IpaC）引发与病原体入侵有关的上皮细胞反应。

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Shigella flexneri invades colonic epithelial cells by pathogen-induced phagocytosis. The three proposed effectors of S. flexneri internalization are invasion plasmid antigens B (IpaB), IpaC, and IpaD, which are encoded on the pathogen's 230-kb virulence plasmid and translocated to the extracellular milieu via the Mxi-Spa translocon. To date, there are no definitive functional data for any purified Ipa protein. Here, we describe the first characterization of highly purified recombinant IpaC, which elicits numerous epithelial cell responses related to events that take place during pathogen invasion. 125I-labeled IpaC binds cultured Henle 407 intestinal cells with an apparent dissociation constant in the low micromolar range. Moreover, incubation of epithelial cells with IpaC results in general changes in cellular phosphoprotein content, demonstrating this protein's ability to influence cellular protein kinase activities. These results contrast dramatically with those seen for recombinant IpaD, which does not bind to or induce detectable changes in the normal activities of cultured epithelial cells. In addition to influencing host cell activities, preincubation of epithelial cells with purified IpaC enhances uptake of S. flexneri by host cells. A similar result is seen when the cells are preincubated with a highly concentrated water extract of virulent S. flexneri 2a (strain 2457T). Interestingly, soluble IpaC also appears to promote uptake of the noninvasive S. flexneri 2a strain BS103. Purified IpaD failed to enhance the uptake of virulent S. flexneri and did not facilitate uptake of BS103. Taken together, the data suggest that IpaC is a potential effector of the host cell biological activities and may be responsible for entry of S. flexneri into target cells.
机译：弗氏志贺氏菌通过病原体诱导的吞噬作用侵入结肠上皮细胞。拟议的弗氏链球菌内在化的三个效应子是侵袭质粒抗原B（IpaB），IpaC和IpaD，它们编码在病原体的230-kb毒力质粒上，并通过Mxi-Spa转座子转移到细胞外环境中。迄今为止，尚无任何纯化的Ipa蛋白的确切功能数据。在这里，我们描述了高度纯化的重组IpaC的第一个特征，它引发了许多与病原体入侵过程中发生的事件相关的上皮细胞反应。 125I标记的IpaC结合培养的Henle 407肠细胞，其表观解离常数在低微摩尔范围内。此外，将上皮细胞与IpaC孵育会导致细胞磷蛋白含量的普遍变化，从而证明该蛋白影响细胞蛋白激酶活性的能力。这些结果与重组IpaD所观察到的结果形成鲜明对比，后者不结合或诱导培养的上皮细胞正常活动中的可检测变化。除了影响宿主细胞的活性外，上皮细胞与纯化的IpaC的预孵育还增强了宿主细胞对弗氏链球菌的吸收。当将细胞与强力弗氏链球菌2a（菌株2457T）的高浓度水提取物预孵育时，会看到类似的结果。有趣的是，可溶性IpaC似乎也促进了非侵入性弗氏链球菌2a菌株BS103的吸收。纯化的IpaD不能增强对强毒链球菌的吸收，也不能促进BS103的吸收。两者合计，数据表明，IpaC是宿主细胞生物学活性的潜在效应器，可能负责弗氏链球菌进入靶细胞。

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