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首页> 外文期刊>Infection and immunity >The Capsule-Encoding viaB Locus Reduces Intestinal Inflammation by a Salmonella Pathogenicity Island 1-Independent Mechanism
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The Capsule-Encoding viaB Locus Reduces Intestinal Inflammation by a Salmonella Pathogenicity Island 1-Independent Mechanism

机译：经由B基因座的胶囊编码通过沙门氏菌致病岛1独立机制减少肠道炎症

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Salmonella enterica serotype Typhimurium elicits acute neutrophil influx in the human intestinal mucosa within 1 or 2 days after infection, resulting in inflammatory diarrhea. In contrast, no overt symptoms are observed within the first 1 or 2 weeks after infection with S. enterica serotype Typhi. Here we show that introduction of the capsule-encoding viaB locus of serotype Typhi reduced the ability of serotype Typhimurium to elicit acute intestinal inflammation in a streptomycin-pretreated mouse model. Serotype Typhimurium requires a functional invasion-associated type III secretion system (type III secretion system 1 [T3SS-1]) to elicit cecal inflammation within 48 h after infection of streptomycin-pretreated mice, and the presence of the viaB locus reduced its invasiveness for human intestinal epithelial cells in vitro. However, a reduced activity of T3SS-1 could not account for the ability of the viaB locus to attenuate cecal inflammation, because introduction of the viaB locus into an invasion-deficient serotype Typhimurium strain (invA mutant) resulted in a significant reduction of pathology and inflammatory cytokine expression in the cecum 5 days after infection of mice. We conclude that a T3SS-1-independent mechanism contributes to the ability of the viaB locus to reduce intestinal inflammation.
机译：鼠伤寒沙门氏菌血清型在感染后1或2天内引起人肠粘膜急性中性粒细胞流入，导致炎症性腹泻。相反，感染 S后的前1或2周内未观察到明显症状。肠型血清型伤寒。在这里，我们表明，在链霉素预处理的小鼠模型中，鼠伤寒血清型的编码 viaB 的胶囊的引入降低了鼠伤寒血清型引起急性肠道炎症的能力。血清型鼠伤寒需要感染链霉菌素的小鼠感染后48小时内以及 viaB 存在的功能性入侵相关的III型分泌系统（III型分泌系统1 [T3SS-1]）引发盲肠炎症。 em>基因座在体外降低了其对人肠上皮细胞的侵袭性。但是，T3SS-1活性降低不能解释 viaB 位点减弱盲肠炎症的能力，因为将 viaB 位点引入侵袭缺陷型鼠伤寒杆菌株（ invA 突变株）导致小鼠感染后5天盲肠的病理和炎症细胞因子表达显着降低。我们得出结论，T3SS-1独立机制有助于 viaB 基因座减少肠道炎症的能力。

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