[Pathogenic factors of mycoplasma].

Takashi Shimizu
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引用次数: 16

Abstract

Mycoplasmas are smallest organisms capable of self-replication and cause various diseases in human. Especially, Mycoplasma pneumoniae is known as an etiological agent of pneumonia. From 2010 to 2012, epidemics of M. pneumoniae infections were reported worldwide (e.g., in France, Israel, and Japan). In the diseases caused by mycoplasmas, strong inflammatory responses induced by mycoplasmas have been thought to be important. However, mycoplasmas lack of cell wall and do not possess inflammation-inducing endotoxin such as lipopolysaccharide (LPS). We purified inflammation-inducing factors from pathogenic mycoplasmas and identified that they were lipoproteins. Lipoproteins derived from mycoplasmas induced inflammatory responses through Toll-like receptor (TLR) 2. In addition, we demonstrated that cytadherent property of M. pneumoniae played an important role in induction of inflammatory responses. Cytadherent property of M. pneumoniae induced inflammatory responses through TLR2 independent pathway. TLR4, inflammasomes, and autophagy were involved in this TLR2 independent induction of inflammatory responses.
[支原体致病因素]。
支原体是具有自我复制能力的最小生物,可引起人类多种疾病。特别是,肺炎支原体被认为是肺炎的病原。2010年至2012年,全球报告了肺炎支原体感染流行(如法国、以色列和日本)。在由支原体引起的疾病中,由支原体引起的强烈炎症反应被认为是重要的。然而,支原体缺乏细胞壁,不具有诱导炎症的内毒素,如脂多糖(LPS)。我们从致病性支原体中纯化了炎症诱导因子,并鉴定出它们是脂蛋白。来自支原体的脂蛋白通过toll样受体(TLR) 2诱导炎症反应。此外,我们证明了肺炎支原体的细胞粘附特性在诱导炎症反应中起重要作用。肺炎支原体通过TLR2非依赖性途径诱导炎症反应的细胞粘附特性。TLR4、炎性小体和自噬参与了这种不依赖TLR2的炎症反应诱导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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