IL-1 receptor regulates S100A8/A9-dependent keratinocyte resistance to bacterial invasion.
IL-1 receptor regulates S100A8/A9-dependent keratinocyte resistance to bacterial invasion.
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我们以前报道过，上皮细胞通过增加参与宿主对微生物反应的几个基因的表达来对外源性IL-1α作出反应，包括抗菌蛋白复合物钙卫蛋白（S100 A8/A9）。鉴于S100 A8/A9保护上皮细胞免受入侵细菌的侵害，我们研究了IL-1α是否增强了S100 A8/A9依赖的口腔角质形成细胞对细菌入侵的抵抗力。当接种单核细胞增生李斯特菌时，人颊上皮细胞（TR 146）表达并释放IL-1α。随后，来自李斯特菌感染细胞的含有IL-1α的培养基以IL-1受体（IL-1 R）依赖性方式增加了幼稚TR 146细胞中S100 A8/A9基因的表达。外源性IL-1α抑制了李斯特菌对TR 146细胞的侵袭，而IL-1 R拮抗剂则增强了李斯特菌对TR 146细胞的侵袭。相反，当使用shRNA敲低S100 A8/A9基因时，TR 146细胞对外源性IL-1α的反应是细胞内细菌增加。这些数据有力地表明，感染的上皮细胞以旁分泌方式释放IL-1α向邻近的角质形成细胞发出信号，促进S100 A8/A9依赖性抵抗侵袭性L.单核细胞增多症。
Previously we reported that epithelial cells respond to exogenous IL-1α by increasing expression of several genes involved in the host response to microbes, including the antimicrobial protein complex calprotectin (S100A8/A9). Given that S100A8/A9 protects epithelial cells against invading bacteria, we studied whether IL-1α augments S100A8/A9-dependent resistance to bacterial invasion of oral keratinocytes. When inoculated with Listeria monocytogenes, human buccal epithelial (TR146) cells expressed and released IL-1α. Subsequently, IL-1α-containing media from Listeria-infected cells increased S100A8/A9 gene expression in naïve TR146 cells an IL-1 receptor (IL-1R)-dependent manner. Incubation with exogenous IL-1α decreased Listeria invasion into TR146 cells, whereas invasion increased with IL-1R antagonist. Conversely, when S100A8/A9 genes were knocked down using shRNA, TR146 cells responded to exogenous IL-1α with increased intracellular bacteria. These data strongly suggest that infected epithelial cells release IL-1α to signal neighboring keratinocytes in a paracrine manner, promoting S100A8/A9-dependent resistance to invasive L. monocytogenes.
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