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首页> 外文期刊>Infection and immunity >Campylobacter jejuni Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2
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Campylobacter jejuni Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2

机译：空肠弯曲杆菌通过Toll样受体2驱动MyD88独立的白介素6分泌

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Gastrointestinal disease caused by Campylobacter jejuni is characterized by localized inflammation and the destruction of the epithelial cell barrier that forms host innate protection against pathogens. This can lead to an imbalance in fluid transport across the gastrointestinal tract, resulting in severe diarrhea. The mechanisms of host cell receptor recognition of C. jejuni and downstream immune signaling pathways leading to this inflammatory disease, however, remain unclear. The aim of this study was to analyze the mechanisms involved in C. jejuni induction of the acute-phase inflammatory response regulator interleukin-6 (IL-6). Polarized intestinal epithelial Caco-2 monolayers responded to infections with Salmonella enterica serovar Typhimurium and eight isolates of C. jejuni by an increase in levels of expression and secretion of IL-6. No such IL-6 response, however, was produced upon infection with the human commensal organism Lactobacillus rhamnosus GG. The IL-6 signaling pathway was further characterized using short interfering RNA complexes to block gene expression. The inhibition of myeloid differentiation primary response protein 88 (MyD88) expression in this manner did not affect C. jejuni-induced IL-6 secretion, suggesting a MyD88-independent route to IL-6 signal transduction in C. jejuni-infected human epithelial cells. However, a significant reduction in levels of IL-6 was evident in the absence of Toll-like receptor 2 (TLR-2) expression, implying a requirement for TLR-2 in C. jejuni recognition. Caco-2 cells were also treated with heat-inactivated and purified membrane components of C. jejuni to isolate the factor responsible for triggering IL-6 signaling. The results demonstrate that C. jejuni surface polysaccharides induce IL-6 secretion from intestinal epithelial cells via TLR-2 in a MyD88-independent manner.
机译：空肠弯曲杆菌引起的胃肠道疾病的特征是局部炎症和上皮细胞屏障的破坏，形成宿主对病原体的先天保护。这可能会导致整个胃肠道的液体运输不平衡，从而导致严重的腹泻。宿主细胞受体识别 C的机制。空肠和下游免疫信号通路导致这种炎症性疾病，但仍不清楚。这项研究的目的是分析参与 C的机制。空肠诱导急性期炎症反应调节剂白细胞介素6（IL-6）。极化的肠上皮Caco-2单层细胞对肠炎沙门氏菌血清鼠伤寒杆菌和八种肠溶菌的感染有反应。空肠通过增加IL-6的表达和分泌水平。然而，在人类共生生物鼠李糖乳杆菌 GG感染后，没有产生这种IL-6反应。使用短干扰RNA复合物阻断基因表达，进一步表征IL-6信号传导途径。以这种方式抑制髓样分化初级反应蛋白88（MyD88）的表达不影响 C。空肠诱导的IL-6分泌，提示 C中MyD88依赖的IL-6信号转导途径。空肠感染的人上皮细胞。但是，在不存在Toll样受体2（TLR-2）表达的情况下，IL-6的水平明显降低，这表明 C中需要TLR-2。空肠识别。 Caco-2细胞也用热灭活和纯化的C膜成分处理。空肠以分离引起IL-6信号触发的因子。结果表明， C。空肠表面多糖以不依赖MyD88的方式通过TLR-2诱导肠上皮细胞分泌IL-6。

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