| Summary: | 碩士 === 國立成功大學 === 醫事技術學系 === 92 === Intracellular bacteria of the genus Chlamydia cause numerous typical chronic diseases, frequently with debilitating sequelae. Persistent chlamydial infections have been proposed as a means whereby Chlamydiae evade immune responses of infection. Altered production of nitric oxide (NO), a known bactericidal and anti-inflammatory agent represents one possible mechanistic link. Smooth muscle cells (SMC) might be important targets for airway remodeling in chronic asthma, bronchitis, and atherogenesis associated with C. pneumoniae. In this study, we evaluate the NO effect on chlamydial infection in SMC. Our results demonstrated that infection of rat aortic SMC, A7r5 cell line with C. pneumoniae resulted in the development of typical inclusion bodies in the cells, similar to those seen in epithelial cells. NO production was inhibited by C. pneumoniae and mediated by down-regulation of eNOS expression. Treatment with NO donor, sodium nitroprusside (SNP) reduced chlamydial inclusion-forming units by 2 log10 units as compared with control values. In contrast, chlamydial growth was enhanced by iNOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). Furthermore, the effect of NO was demonstrated to be more specifically important in the early phase of chlamydial development (<24 hours). The analysis of bacterial messenger RNA in the cultures showed that the expression ratio of omcB/hsp60 was down-regulated by SNP and it was also dose-dependent, whereas the expression ratio was not changed by L-NAME treatment. In conclusion, our preliminary data suggests that chlamydial growth in SMC inhibit NO production, which is a necessary effecter molecule involved in the early phase of chlamydial development. However, the role of NO donor as an antichlamydial effector should be clarified by further investigation.
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