| Summary: | 碩士 === 國立成功大學 === 醫學檢驗生物技術學系碩博士班 === 97 === Infection with the Chlamydia trachomatis can lead to a variety of chronic inflammatory diseases. Two components, Chlamydial lipopolysaccharide (LPS) and heat shock protein 60 (cHSP60), that can bind to CD14, a glycosylphosphatidyl-inositol-anchored membrane protein, and activate macrophages to induce inflammatory responses, which have been shown implicated in the pathogenesis of chronic inflammatory chlamydial diseases. Our previous studies have shown that the CD14 functional gene polymorphism -260C>T is associated with CD14 expression and Chlamydia-stimulated TNF-α production. Thus, the purpose of this study is to investigate the specific roles of CD14 in C trachomatis infection and inflammatory responses. The results demonstrated that infectivity of C trachomatis is significantly higher in CD14 over-expressed CHO (CHO/CD14) cell lines. Blockade of surface CD14 using anti-CD14 could reduce the C trachomatis infectivity. We found the internalization activity of C trachomatis is higher in CHO/CD14 than CHO/pCR3 cells, and the results were similar in PMA-treated U937 cells. In addition, Chlamydia infection dose-dependently increased NF-κB reporter activity in CHO/CD14 cells compared with CHO/pCR3. The effect of CD14 on NF-κB activation was enhanced by TLR2 cotransfection. Furthermore, we have demonstrated Chlamydial HSP60 but not LPS to enhance NF-κB transactivation by CD14-dependent manner after C trachomatis infection. In conclusion, CD14 plays an important role in C trachomatis internalization to enhance infectivity. The HSP60 which is produced by Chlamydia proliferation, is the most important component to induce CD14-mediated NF-κB activation during C trachomatis infection
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