Effect of nitric oxide on the growth of Chlamydophila pneumoniae
Effect of nitric oxide on the growth of Chlamydophila pneumoniae
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DOI：
10.1139/w05-080
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发表时间：
2005-11-01
影响因子：
2.8
通讯作者：
Rossano, F
中科院分区：
文献类型：
--
作者：
Carratelli, CR;Rizzo, A;Rossano, F
肺炎衣原菌是一种重要的人类细胞内病原体，然而，肺炎衣原菌感染的发病机制尚不清楚，对宿主细胞的免疫控制机制也不完全清楚。研究一氧化氮（NO）合成酶途径在抑制肺炎原体感染巨噬细胞J774细胞中的作用以及NO对分离的肺炎原体的损伤能力。将受感染的培养物暴露于重组小鼠γ干扰素（murifn - γ）中导致NO的产生增加和生存能力降低。在感染J774细胞前或在衣原体培养过程中添加2-（N，N-二乙胺）-重氮醇酶-2-氧化物释放NO，两者均导致肺炎C的生存能力呈剂量依赖性降低。这些结果表明，免疫控制小鼠巨噬细胞中衣原体的生长可能触发一种机制，其中包括NO的释放，并影响微生物的增殖，从而提示NO可能在阻止衣原体的全身传播中发挥作用。
Chlamydophila pneumoniae is an important human intracellular pathogen: however, the pathogenesis of C. pneumoniae infection is poorly understood and the immune control mechanism versus host cells is not completely known. The role of the nitric oxide (NO) synthase pathway in inhibiting the ability of C. pneumoniae to infect macrophage J774 cells and the ability of NO to damage isolated C. pneumoniae were investigated. Exposure of infected cultures to recombinant murine gamma interferon (MurIFN-gamma) resulted in increased production of NO and reduced viability. Addition of 2-(N,N-diethylamino)-diazenolase-2-oxide before infection of J774 cells or during chlamydial cultivation released NO, both resulting in a reduction in the viability of C pneumoniae in a dose-dependent way. These results indicate that immune control of chlamydial growth in murine macrophage cells may trigger a mechanism that includes NO release with effects on the multiplication of the microorganism, thus suggesting that NO may play a role in preventing the systemic spread of Chlamydia.