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首页> 外文期刊>American Journal of Physiology >Innate immune responses of human tracheal epithelium to Pseudomonas aeruginosa flagellin, TNF-alpha, and IL-1beta.
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Innate immune responses of human tracheal epithelium to Pseudomonas aeruginosa flagellin, TNF-alpha, and IL-1beta.

机译：人气管上皮对铜绿假单胞菌鞭毛蛋白，TNF-α和IL-1β的先天免疫应答。

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We measured innate immune responses by primary human tracheal epithelial (HTE) cells grown as confluent, pseudostratified layers during exposure to inflammatory activators on apical vs. basolateral surfaces. Apical Pseudomonas aeruginosa strain PAK (but not flagellin mutant PAK.fliC), flagellin, and flagellin + PAK.fliC activated NF-kappaB and IL-8 expression and secretion. In contrast, HTE cells were insensitive to LPS compared to flagellin. Flagellin activated NF-kappaB in columnar but not basal cells. IL-1beta + TNF-alpha elicited responses similar to those of flagellin. Basolateral flagellin or IL-1beta + TNF-alpha caused 1.5- to 4-fold larger responses, consistent with the fact that NF-kappaB activation occurred in both columnar and basal cells. MyD88 (toll receptor-associated adapter), IL-1 receptor (IL1R)1, and TNF-alpha receptor (TNFR)1 were expressed in columnar and basal cells. ZO-1 was localized to tight junctions of columnar cells but not to basal cells. We infer the following. 1) Flagellinis necessary and sufficient to trigger inflammatory responses in columnar cells during accumulation of P. aeruginosa in the airway surface liquid (ASL); columnar cells express toll-like receptor 5 and MyD88, often associated with flagellin-activated cell signaling. 2) IL-1beta + TNF-alpha in the ASL also activate columnar cells, and these cells also express IL1R1 and TNFR1. 3) Apical flagellin, IL-1beta, and TNF-alpha do not activate basal cells because tight junctions between columnar cells prevent access from the apical surface to the basal cells. 4) Exposure of basolateral surfaces to inflammatory activators elicits larger responses because both columnar and basal cells are activated, likely because both cell types express receptors for flagellin, IL-1beta, and TNF-alpha.
机译：我们通过暴露于根尖和基底外侧表面上的炎性激活剂期间生长为汇合的伪分层层的原代人气管上皮细胞（HTE）来测量先天免疫应答。顶端的铜绿假单胞菌菌株PAK（但不是鞭毛蛋白突变体PAK.fliC），鞭毛蛋白和鞭毛蛋白+ PAK.fliC激活了NF-κB和IL-8的表达和分泌。相反，与鞭毛蛋白相比，HTE细胞对LPS不敏感。鞭毛蛋白可激活柱状细胞但不激活基底细胞中的NF-κB。 IL-1beta +TNF-α引起的反应类似于鞭毛蛋白。基底外侧鞭毛蛋白或IL-1β+TNF-α引起1.5至4倍大的应答，这与柱状和基底细胞中都发生NF-κB活化的事实一致。 MyD88（收费受体相关的适配器），IL-1受体（IL1R）1和TNF-α受体（TNFR）1在柱状和基底细胞中表达。 ZO-1定位在柱状细胞的紧密连接处，而不是基底细胞。我们推断如下。 1）在铜绿假单胞菌在气道表面液体（ASL）积累期间触发柱状细胞中炎症反应的必要和充分的鞭毛;柱状细胞表达toll样受体5和MyD88，通常与鞭毛蛋白激活的细胞信号传导有关。 2）ASL中的IL-1beta +TNF-α也激活柱状细胞，这些细胞也表达IL1R1和TNFR1。 3）顶端鞭毛蛋白，IL-1β和TNF-α不会激活基底细胞，因为柱状细胞之间的紧密连接会阻止从顶端表面进入基底细胞。 4）基底外侧表面暴露于炎性激活剂会引起更大的反应，因为柱状细胞和基底细胞均被激活，这可能是因为两种细胞类型均表达鞭毛蛋白，IL-1β和TNF-α的受体。

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