Investigation of oral mucosal inflammatory disease developing mechanism via Toll-like receptor

口腔角化细胞和成纤维细胞可能增强宿主防御和炎症反应，以抵抗口腔微生物的入侵。然而，目前尚不清楚口腔角化细胞和成纤维细胞是否在病原体相关分子模式（pathogen associated molecular patterns， PAMPS）的反应中产生特异性炎症蛋白，并与口腔黏膜炎症性疾病相关。结果表明，口腔角质形成细胞和成纤维细胞表达TLRs 1-10的mRNA。各种TLR激动剂可诱导口腔角质形成细胞和成纤维细胞产生IL-8和CXCL10。这些发现表明，TLR对口腔角质形成细胞和成纤维细胞中微生物来源的病原体的识别可能在协调宿主免疫反应和通过产生各种趋化因子促进与口腔炎症疾病相关的高/低反应中发挥重要作用。

Oral keratinocytes and fibroblasts may augment host defense and inflammatory responses against oral microorganisms invasion. However, it remains unclear whether oral keratinocytes and fibroblasts produce specific inflammatory proteins in response to Pathogen-associated molecular patterns (PAMPS) and associated with oral mucosal inflammatory diseases. Our results showed that oral keratinocytes and fibroblasts expressed mRNA of TLRs 1-10. IL-8 and CXCL10 production from oral keratinocytes and fibroblasts was induced by treatment with various TLR agonisits. These findings suggest that recognition of microorganism-derived pathogen in oral keratinocytes and fibroblasts by TLR may have important role to orchestrate host immune responses and promoting hyper/hypo reactions related to oral inflammatory diseases via production of various chemokines.