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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Bacterial chemotaxis modulates host cell apoptosis to establish a T-helper cell, type 17 (Th17)-dominant immune response in Helicobacter pylori infection
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Bacterial chemotaxis modulates host cell apoptosis to establish a T-helper cell, type 17 (Th17)-dominant immune response in Helicobacter pylori infection

机译：细菌趋化性调节宿主细胞凋亡，从而在幽门螺杆菌感染中建立以T型辅助细胞为主的17（Th17）型免疫应答

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The host inflammatory response to chronic bacterial infections often dictates the disease outcome. In the case of the gastric pathogen Helicobacter pylori, host inflammatory responses result in outcomes that range from moderate and asymptomatic to more severe with concomitant ulcer or cancers. It was found recently that H. pylori chemotaxis mutants (Che-), which lack directed motility but colonize to nearly wild-type levels, trigger less host inflammation. We used these mutants to observe host immune responses that resulted in reduced disease states. Here we report that these mutants are defective for early gastric recruitment of CD4+ T cells compared with wild-type infection. Furthermore, Che" mutant infections lack the T-helper cell, type 17 (Th17) component of the immune response, as measured by cytokine mRNA levels in gastric tissue via intracellular cytokine Staining and immunofluorescence. We additionally find that a Che~ mutant infection results in significantly less host cell apoptosis than does wild-type infection, in accordance with previous observations that T-helper cell, type 17 responses in Citrobacter rodentium infections are driven by concomitant bacterial and apopto-tic cell signals. We propose that bacterial chemotaxis allows H. pylori to access a particular host niche that allows the bacteria to express or deliver proapoptotic host cell factors. This report indicates that chemotaxis plays a role in enhancing apoptosis, suggesting bacterial chemotaxis systems might serve as therapeutic targets for infections whose symptoms arise from host cell apoptosis and tissue damage.
机译：宿主对慢性细菌感染的炎症反应通常决定了疾病的结局。在胃病原体幽门螺杆菌的情况下，宿主的炎症反应导致的结果范围从中度和无症状到伴随溃疡或癌症的更严重。最近发现，幽门螺杆菌趋化性突变体（Che-）缺乏定向运动能力，但定居到接近野生型水平，触发的宿主炎症更少。我们使用这些突变体观察导致疾病状态降低的宿主免疫反应。在这里我们报告这些突变体与野生型感染相比早期胃募集的CD4 + T细胞有缺陷。此外，通过细胞内细胞因子染色和免疫荧光检测胃组织中的细胞因子mRNA水平，“ Che”突变型感染缺乏免疫应答的T辅助细胞，即17型（Th17）成分。我们还发现，Che〜突变型感染会导致根据以前的观察，啮齿类柠檬酸杆菌感染中的T型辅助细胞，17型应答是由伴随的细菌和凋亡细胞信号驱动的，因此宿主细胞的凋亡明显少于野生型感染。幽门螺杆菌进入特定的宿主环境，使细菌能够表达或传递促凋亡的宿主细胞因子，该报告表明趋化性在增强细胞凋亡中发挥作用，这表明细菌趋化性系统可以作为症状的宿主，这些感染的病因是宿主细胞细胞凋亡和组织损伤。

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