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首页> 美国卫生研究院文献>Infection and Immunity >The Vi Capsular Antigen of Salmonella enterica Serotype Typhi Reduces Toll-Like Receptor-Dependent Interleukin-8 Expression in the Intestinal Mucosa
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The Vi Capsular Antigen of Salmonella enterica Serotype Typhi Reduces Toll-Like Receptor-Dependent Interleukin-8 Expression in the Intestinal Mucosa

机译：肠沙门氏菌血清型伤寒沙门氏菌的Vi胶囊抗原降低Toll样受体依赖性白细胞介素8在肠粘膜中的表达。

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Human infections with nontyphoidal Salmonella serotypes, such as S. enterica serotype Typhimurium, are characterized by a massive neutrophil influx in the colon and terminal ileum. In contrast, neutrophils are scarce in intestinal infiltrates of typhoid fever patients. Here, we show that in S. enterica serotype Typhi, the causative agent of typhoid fever, expression of the Vi capsular antigen reduced expression of the neutrophil chemoattractant interleukin-8 (IL-8) in host cells. Capsulated bacteria elicited IL-8 expression in polarized human epithelial cells (T84) and human macrophage-like cells (THP-1) in vitro at significantly reduced levels compared to noncapsulated bacteria. Experiments with a human cell line (HEK293) transfected with human Toll-like receptors (TLRs) demonstrated that in the presence of TLR5 or TLR4/MD2/CD14, a noncapsulated serotype Typhi mutant was able to induce the expression of IL-8, while this host response was significantly reduced when cells were infected with the capsulated serotype Typhi wild type. The relevance of these in vitro observations for the interaction of serotype Typhi with its human host was further studied ex vivo using human colonic tissue explants. Expression of IL-8 was detected in human colonic tissue explants infected with serotype Typhimurium or a noncapsulated serotype Typhi mutant. In contrast, infection with the serotype Typhi wild type did not elicit IL-8 expression in colonic tissue explants. Collectively, these data suggest that the scarcity of neutrophils in intestinal infiltrates of typhoid fever patients is due to a capsule-mediated reduction of TLR-dependent IL-8 production in the intestinal mucosa.
机译：非伤寒沙门氏菌血清型（例如肠炎链球菌血清型鼠伤寒）的人类感染的特征是结肠和回肠末端大量嗜中性粒细胞大量涌入。相反，伤寒患者肠道浸润中性粒细胞稀少。在这里，我们显示出在伤寒沙门氏菌血清型伤寒沙门氏菌中，Vi荚膜抗原的表达降低了宿主细胞中性粒细胞趋化因子白细胞介素8（IL-8）的表达。与未包被的细菌相比，被包被的细菌在体外在极化的人上皮细胞（T84）和人巨噬细胞样细胞（THP-1）中引起IL-8表达，且水平明显降低。用人类Toll样受体（TLR）转染的人类细胞系（HEK293）进行的实验表明，在存在TLR5或TLR4 / MD2 / CD14的情况下，非封装的血清型Typhi突变体能够诱导IL-8的表达，而当用荚膜血清型Typhi野生型感染细胞时，这种宿主反应显着降低。使用人结肠组织外植体离体进一步研究了这些体外观察与血清型伤寒与其人类宿主相互作用的相关性。在感染了鼠伤寒血清型或鼠伤寒非突变型血清的人结肠组织外植体中检测到IL-8的表达。相反，血清型Typhi野生型感染并未在结肠组织外植体中引起IL-8表达。总的来说，这些数据表明伤寒患者肠道浸润中嗜中性粒细胞的缺乏是由于胶囊介导的肠粘膜中TLR依赖性IL-8产生的减少。

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