Program for Applied Biomedicine, Division of Cervico-Gnathostmatology, Department of Oral and Maxillofacial Surgery, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-Ku, Hiroshima, 734-8553, Japan.
Microbiol Immunol. 2013 Mar;57(3):198-206. doi: 10.1111/1348-0421.12022.
Oral keratinocytes and fibroblasts may be the first line of host defense against oral microorganisms. Here, the contention that oral keratinocytes and fibroblasts recognize microbial components via Toll-like receptors (TLRs) and participate in development of oral inflammation was examined. It was found that immortalized oral keratinocytes (RT7), fibroblasts (GT1) and primary cells express mRNA of TLRs 1-10. Interleukin-8 (IL-8) production by RT7 cells was induced by treatment with TLRs 1-9 with the exception of TLR7 agonist, whereas GT1 cells were induced to produce IL-8 by all TLR agonists tested except for TLR7 and TLR9. GT1 cells showed increased CXCL10 production following treatment with agonists for TLR1/2, TLR3, TLR4, and TLR5, whereas only those for TLR3 and TLR5 increased CXCL10 production in RT7 cells. Moreover, TLR agonists differentially regulated tumor necrosis factor-alpha-induced IL-8 and CXCL10 production by the tested cell types. These findings suggest that recognition of pathogenic microorganisms in oral keratinocytes and fibroblasts by TLRs may have important roles in orchestrating host immune responses via production of various chemokines.
口腔角质细胞和纤维母细胞可能是宿主第一道防线，用以抵御口腔微生物。在此，我们探讨了口腔角质细胞和纤维母细胞是否通过 Toll 样受体 (TLR) 识别微生物成分并参与口腔炎症发生的问题。结果发现，永生化口腔角质细胞 (RT7)、纤维母细胞 (GT1) 和原代细胞表达 TLR1-10 的 mRNA。TLR1-9 激动剂可诱导 RT7 细胞产生白细胞介素-8 (IL-8)，但 TLR7 激动剂除外，而所有测试的 TLR 激动剂均可诱导 GT1 细胞产生 IL-8，TLR7 和 TLR9 除外。TLR1/2、TLR3、TLR4 和 TLR5 的激动剂可诱导 GT1 细胞产生 CXCL10，而仅 TLR3 和 TLR5 的激动剂可诱导 RT7 细胞产生 CXCL10。此外，TLR 激动剂可通过不同方式调节 TNF-α诱导的 IL-8 和 CXCL10 产生。这些发现提示，TLR 对口腔角质细胞和纤维母细胞中致病性微生物的识别可能通过产生各种趋化因子在调控宿主免疫反应中发挥重要作用。
