Abnormal pattern recognition receptor (PRR) signaling plays an important role in gastric mucosal damage caused by stomach microbiota; however, the underlying molecular mechanisms remain obscure. Here, we show that DC-SIGN, a surface phenotype marker of dendritic cells, is overexpressed in gastric epithelial cells facing LPS stimulation. NLRP3 expression in gastric epithelial cells are significantly increased and related to the degree of LPS stimulation. Furthermore, DC-SIGN could interact with TLR4, promote NLRP3 and related genes expression via MyD88-independent signaling pathway and regulate the secretion of IL-1β and IL-18 in gastric epithelial cells. The results of flow cytometry analysis show that DC-SIGN primarily mediates Th1 differentiation when co-cultured with gastric epithelial cells. These results reveal that LPS-induced DC-SIGN expression modulates NLRP3 inflammasomes formation via MyD88-independent TLR4 signaling in gastric epithelial cell, and induces a Th1-predominant host immune response,these findings may indicate a new function of DC-SIGN in non-immune cells, and elucidate the diversity role of gastric epithelial cells in mechanism of immune damage caused by microbial flora.

异常模式识别受体（PRR）信号在胃微生物群引起的胃粘膜损害中起重要作用。然而，潜在的分子机制仍然不清楚。在这里，我们显示DC-SIGN，树突状细胞的表面表型标记，在面对LPS刺激的胃上皮细胞中过表达。胃上皮细胞中的NLRP3表达显着增加，并与LPS刺激的程度有关。此外，DC-SIGN可以通过不依赖MyD88的信号通路与TLR4相互作用，促进NLRP3和相关基因的表达，并调节胃上皮细胞中IL-1β和IL-18的分泌。流式细胞仪分析结果表明，DC-SIGN与胃上皮细胞共培养时主要介导Th1分化。