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探讨固有免疫分子DC-SIGN在幽门螺杆菌(H.pylori)感染的胃上皮细胞表达,及其与胃黏膜损伤的关系。选取经胃镜及组织病理检查确诊的72例慢性胃炎患儿胃黏膜活检标本,采用免疫组化检测胃黏膜上皮细胞DC-SIGN表达。体外建立幽门螺杆菌感染胃上皮细胞模型,采用流式细胞术检测幽门螺杆菌刺激的胃上皮细胞DC-SIGN以及CD80、CD86表达;ELISA测定胃上皮细胞与CD4+T细胞共培养后上清中IFN-γ、IL-4的含量。结果显示,慢性胃炎患者胃黏膜上皮细胞可见DC-SIGN表达,其中幽门螺杆菌感染阳性患者显高于阴性者(P<0.01),并随胃黏膜炎症程度加重DC-SIGN表达增强(P<0.01),显示与幽门螺杆菌感染明显相关(P<0.01)。此外发现,幽门螺杆菌体外可刺激胃上皮细胞上调表达DC-SIGN、CD86,且经幽门螺杆菌处理的胃上皮细胞可诱导CD4+T细胞IFN-γ分泌增多(P<0.01);经抗DC-SIGN单抗干预,可抑制DC-SIGN并相应下调CD86表达,且IFN-γ分泌减少及IFN-γ/IL-4比值下降(P<0.01、P<0.05)。结果表明,幽门螺杆菌感染的胃黏膜上皮细胞也表达树突状细胞(DC)表型DC-SIGN,并具有诱导T细胞向Th1分化为主的DC样细胞功能;DC-SIGN可能在介导胃上皮细胞于幽门螺杆菌胃黏膜损伤机制中发挥重要作用。
To investigate the expression of innate immune molecule DC-SIGN in gastric epithelial cells infected with H.pylori and its relationship with gastric mucosal injury. Gastric mucosal biopsy specimens from 72 children with chronic gastritis diagnosed by gastroscopy and histopathology were selected and the expression of DC-SIGN in gastric mucosal epithelial cells was detected by immunohistochemistry. The H.pylori-infected gastric epithelial cell model was established in vitro. DC-SIGN, CD80 and CD86 expression of gastric epithelial cells stimulated by Helicobacter pylori were detected by flow cytometry. The expression of CD80 and CD86 in gastric epithelial cells stimulated by H.pylori was detected by ELISA. IFN-γ, IL-4 content. The results showed that DC-SIGN expression was found in gastric mucosal epithelial cells of patients with chronic gastritis, and the positive rate of Helicobacter pylori infection in patients with chronic Helicobacter pylori infection was significantly higher than that in negative ones (P <0.01). The expression of DC-SIGN was enhanced with the degree of gastric mucosal inflammation (P <0.01) ), Showed significant correlation with Helicobacter pylori infection (P <0.01). In addition, it was found that H. pylori could upregulate the expression of DC-SIGN and CD86 in gastric epithelial cells in vitro, and that gastric epithelial cells treated with Helicobacter pylori could induce an increase of IFN-γ secretion of CD4 + T cells (P <0.01) DC-SIGN monoclonal antibody could inhibit DC-SIGN and down-regulate the expression of CD86, decrease the secretion of IFN-γand decrease the ratio of IFN-γ / IL-4 (P <0.01, P <0.05). The results showed that H. pylori-infected gastric mucosal epithelial cells also expressed dendritic cell (DC) phenotype DC-SIGN and had the function of inducing T cells to differentiate into DC-like cells. DC-SIGN may be mediated Gastric epithelial cells play an important role in the mechanism of gastric mucosal injury in Helicobacter pylori.