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首页> 外文期刊>Infection and immunity >Yersinia enterocolitica-Induced Interleukin-8 Secretion by Human Intestinal Epithelial Cells Depends on Cell Differentiation
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Yersinia enterocolitica-Induced Interleukin-8 Secretion by Human Intestinal Epithelial Cells Depends on Cell Differentiation

机译：人肠上皮细胞小肠结肠炎耶尔森菌诱导的白介素8分泌取决于细胞分化。

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In response to bacterial entry epithelial cells up-regulate expression and secretion of various proinflammatory cytokines, including interleukin-8 (IL-8). We studied Yersinia enterocolitica O:8-induced IL-8 secretion by intestinal epithelial cells as a function of cell differentiation. For this purpose, human T84 intestinal epithelial cells were grown on permeable supports, which led to the formation of tight monolayers of polarized intestinal epithelial cells. To analyze IL-8 secretion as a function of cell differentiation, T84 monolayers were infected from the apical or basolateral side at different stages of differentiation. Both virulent (plasmid-carrying) and nonvirulent (plasmid-cured) Y. enterocolitica strains invaded nondifferentiated T84 cells from the apical side. Yersinia invasion into T84 cells was followed by secretion of IL-8. After polarized differentiation of T84 cells Y. enterocolitica was no longer able to invade from the apical side or to induce IL-8 secretion by T84 cells. However,Y. enterocolitica invaded and induced IL-8 secretion by polarized T84 cells after infection from the basolateral side. Basolateral invasion required the presence of the Yersiniainvasion locus, inv, suggesting β1integrin-mediated cell invasion. After basolateral infection,Yersinia-induced IL-8 secretion was not strictly dependent on cell invasion. Thus, although the plasmid-carrying Y. enterocolitica strain did not significantly invade T84 cells, it induced significant IL-8 secretion. Taken together, these data show that Yersinia-triggered IL-8 secretion by intestinal epithelial cells depends on cell differentiation and might be induced by invasion as well as by basolateral adhesion, suggesting that invasion is not essential for triggering IL-8 production. Whether IL-8 secretion is involved in the pathogenesis ofYersinia-induced abscess formation in Peyer’s patch tissue remains to be shown.
机译：响应细菌进入，上皮细胞上调各种促炎细胞因子（包括白介素8（IL-8））的表达和分泌。我们研究了肠上皮细胞小肠结肠炎耶尔森菌 O：8诱导的IL-8分泌与细胞分化的关系。为了这个目的，人T84肠上皮细胞在可渗透的支持物上生长，这导致极化的肠上皮细胞的紧密单层的形成。为了分析IL-8分泌与细胞分化的关系，在分化的不同阶段从顶端或基底外侧感染了T84单层膜。毒性（携带质粒的）和非毒性（经过质粒固化的）Y都是。肠结肠菌菌株从顶端侵袭未分化的T84细胞。 耶尔森氏菌侵入T84细胞后，分泌IL-8。在极化分化的T84细胞后， Y。肠结肠炎不再能够从顶侧侵袭或诱导T84细胞分泌IL-8。但是，是。从基底外侧感染后，极化的T84细胞侵袭小肠结肠炎并诱导IL-8分泌。基底外侧浸润需要存在耶尔森氏菌浸润位点 inv ，提示β 1 整合素介导的细胞浸润。基底外侧感染后，耶尔森氏菌诱导的IL-8分泌并不严格依赖于细胞侵袭。因此，尽管携带质粒的是Y。肠结肠炎菌株没有显着侵袭T84细胞，它诱导了IL-8的大量分泌。综上所述，这些数据表明肠上皮细胞通过耶尔森氏菌触发的IL-8分泌取决于细胞分化，并且可能由浸润以及基底外侧粘连诱导，表明浸润不是触发的必要条件IL-8生产。 IL-8分泌是否与Peyer斑块组织中的耶尔森菌诱导的脓肿形成有关。

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