Chlamydia pneumoniae infection of alveolar macrophages:: A model
Chlamydia pneumoniae infection of alveolar macrophages:: A model
复制标题
DOI：
10.1086/368168
复制
发表时间：
2003-04-01
影响因子：
6.4
通讯作者：
Yamamoto, Y
中科院分区：
文献类型：
--
作者：
Haranaga, S;Yamaguchi, H;Yamamoto, Y
肺炎衣原体是一种常见的呼吸道病原体，肺泡巨噬细胞在肺炎衣原体感染中可能起重要作用。在本研究中，我们检查了小鼠肺泡巨噬细胞的连续细胞系（命名为“MH-S”）作为体外C. pneumoniae感染模型。用C. pneumoniae感染导致细胞中典型包涵体的发展，类似于在原代肺泡巨噬细胞中所见。然而，我们注意到，尽管在感染过程中培养物中的细菌数量增加，但感染性原体的产生受到限制。对培养物中细菌信使RNA的分析表明，omcB基因的信息水平仅处于中等水平，但hsp 60信息水平在感染期间显著增加。通过接种抗体诱导的肿瘤坏死因子（TNF）-α的中和显著增强了感染，但omcB信息水平仍然受到抑制。这些结果表明C.肺泡巨噬细胞中的肺炎可能受到限制。内源性TNF-α可能是导致这种限制的因素之一，但也可能涉及其他因素。
Chlamydia ( Chlamydophila) pneumoniae is a common respiratory pathogen, and it seems likely that alveolar macrophages may have an important role in infection with this bacterium. In the present study, we examined the usefulness of a continuous cell line of murine alveolar macrophages, designated "MH-S," as an in vitro C. pneumoniae infection model. Infection of MH-S cells with C. pneumoniae resulted in the development of typical inclusion bodies in the cells, similar to that seen in primary alveolar macrophages. However, we noted that, although the number of bacteria in the cultures increased during the infection, there was a restricted production of infective elementary bodies. The analysis of bacterial messenger RNA in the cultures showed that the message levels for the omcB gene were present only at a moderate level, but the levels of hsp60 messages increased markedly during infection. Neutralization of tumor necrosis factor (TNF)-alpha induced by inoculation with antibody significantly enhanced the infection, but omcB message levels were still inhibited. These results indicate that the growth of C. pneumoniae in alveolar macrophages may be restricted. Endogenous TNF-alpha may be one of the factors responsible for such restriction, but other factors also may be involved.