Analysis of the interaction between periodontopathic bacteria and junctional epithelial cells using in situ (RT-) PCR

我们研究了牙周致病菌和牙周连接上皮细胞之间的相互作用。RT-PCR结果显示，腐蚀艾克勒氏菌可诱导牙周上皮细胞IL-8、IL-6、PGHS-2 mRNA的表达。有趣的是，用E. KB细胞IL-8、IL-6、PGHS-2 mRNA水平明显升高。这些结果表明，E.与口腔上皮细胞的腐蚀不一定是IL-6、IL-8和前列腺素E2刺激所必需的。我们建议E.为了阐明嗜中性粒细胞通过上皮细胞迁移的机制，我们研究了E.会腐蚀感情RT-PCR检测ICAM-1 mRNA ...更多信息 暴露于E.腐蚀并持续12小时的研究期。此外，抑制E. N-乙酰基-D-半乳糖胺（GalNAc）对KB细胞的腐蚀可降低ICAM-1的表达和纯化的E. Corrodens（GalNAc特异性凝集素样物质，EcLS）增加上皮细胞上ICAM-1的表达。这些结果表明，EcLS在牙龈上皮细胞表达ICAM-1中起关键作用。腐蚀的，我们检查了组件被磷酸化的附件E。腐蚀成上皮细胞Western blot检测到磷酸化p42/44 MAK激酶，但未检测到磷酸化EGF受体。免疫组化结果显示，p42/44 MAP激酶磷酸化产物主要分布于上皮细胞，而结缔组织未见表达。此外，MAP激酶抑制剂阻断ICAM-1和IL-8的表达。综上所述，E. corrotens和EcLS可以通过p42/44 MAP激酶介导与上皮细胞相互作用。少

We examined the interaction between periodontopathic bacteria and periodontal junctional epithelial cells. In RT-PCR, Significant IL-8, IL-6, PGHS-2 mRNA levels were induced from epithelial cells in response to exposure to periodontopahtic Eiklenella corrodens . Interestingly, After incubation with E. corrodens supernatant, KB cells showed marked increase in the levels of IL-8, IL-6, PGHS -2 mRNA. These results imply that the direct contact of E. corrodens with oral epithelial cells is not necessarily required for the sirumulation pf IL-6, IL-8, and Prostaglamdin E2. We suggest that E. corrodens induces the epithelial cells to secrete proinflammatory cyotkines which serve as an early signaling system to host immune and inflammatory cells in underlying conective tissue.To elucidate the mechanism of the transmigration neutrophils through the epithelium, we investigated the expression of adhesion molecules on epithelial cells in response to E. corrodens attachment. In RT-PCR, ICAM-1 mRNA … More levels were significantly increased within 1h in response to exposure to E. corrodeens and continued over the 12h period of study. Furthermore, inhibition of the attachment of E. corrodens to KB cells with N-acetyl-D-galactosamine (GalNAc) decreased the expression of ICAM-1 and purified adhesin of E. corrodens (GalNAc specific lectin like substance, EcLS) increased the ICAM-1 expression on epithelial cells. These findings show that EcLS plays the key role in ICAM-1 expression on gingival epithelial cells.To clarify the signal transduction in KB cells after infection of E. corrodens, we examined components that were phosphrylated by the attachment of E. corrodens to epithelial cells. In western blot analysis, phosphorylated p42/44MAK kinase was detected but phosphorylated EGF receptor was not detected. In histoimmunologycal study, phosphorylated p42/44MAP kinase were detected in epithelium but not connective tissues. Furthermore, inhibitors of MAP kinase blocked the expression of ICAM-1 and IL-8. In summary, secreted proteins from E. corrodens and EcLS can interact with epithelial cells mediating with p42/44 MAP kinase. Less