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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Cytoadherence-dependent induction of inflammatory responses by Mycoplasma pneumoniae.
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Cytoadherence-dependent induction of inflammatory responses by Mycoplasma pneumoniae.

机译：细胞粘附依赖性诱导的肺炎支原体引起的炎症反应。

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Pathogenesis of Mycoplasma pneumoniae infection is considered to be in part attributed to excessive immune responses. Mycoplasma pneumoniae shows strong cytoadherence to host cells and this cytoadherence is thought to be involved in the progression of pneumonia. However, the interaction between the cytoadherence and the immune responses is not known in detail. In this study, we demonstrated that the induction of pro-inflammatory cytokines in the human monocyte cell line THP-1 is dependent on the property of cytoadherence of M. pneumoniae. A wild-type strain of M. pneumoniae with cytoadherence ability induced pro-inflammatory cytokines such as tumour necrosis factor-alpha and interleukin-1beta (IL-1beta). Whereas, heat-killed M. pneumoniae and cytoadherence-deficient mutants of M. pneumoniae caused significantly less production of pro-inflammatory cytokines than the wild-type strain. The wild-type strain induced pro-inflammatory cytokines in an endocytosis-independent manners, but the induction by heat-killed M. pneumoniae and cytoadherence-deficient mutants was dependent on endocytosis. Moreover, the wild-type strain induced caspase-1 production and ATP efflux, promoting the maturation of IL-1beta and release of the pro-IL-1beta precursor, whereas heat-killed M. pneumoniae and the cytoadherence-deficient mutants failed to induce them. These data suggest that the cytoadherence ability of M. pneumoniae activates immune responses and is involved in the pathogenesis of M. pneumoniae infection.
机译：肺炎支原体感染的发病机理被认为部分归因于过度的免疫反应。肺炎支原体对宿主细胞表现出强烈的细胞粘附性，这种细胞粘附性被认为与肺炎的进展有关。但是，细胞粘附和免疫反应之间的相互作用尚不清楚。在这项研究中，我们证明了人类单核细胞系THP-1中促炎性细胞因子的诱导取决于肺炎支原体的细胞粘附特性。具有细胞粘附能力的肺炎支原体的野生型菌株诱导促炎性细胞因子，例如肿瘤坏死因子-α和白介素-1β（IL-1β）。而热灭活的肺炎支原体和缺乏肺炎支原体的突变体引起的促炎性细胞因子的产生比野生型菌株明显少。野生型菌株以不依赖内吞作用的方式诱导促炎性细胞因子，但是热杀死的肺炎支原体和细胞粘附缺陷型突变体的诱导依赖于内吞作用。此外，野生型菌株诱导caspase-1的产生和ATP外排，促进IL-1beta的成熟和pro-IL-1beta前体的释放，而热灭活的肺炎支原体和缺乏细胞粘附性的突变体则无法诱导他们。这些数据表明肺炎支原体的细胞粘附能力激活了免疫应答，并参与了肺炎支原体感染的发病机理。

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