[支原体致病因素]。

Takashi Shimizu
{"title":"[支原体致病因素]。","authors":"Takashi Shimizu","doi":"10.3412/jsb.70.369","DOIUrl":null,"url":null,"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.","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"376 1","pages":"369-74"},"PeriodicalIF":0.0000,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"16","resultStr":"{\"title\":\"[Pathogenic factors of mycoplasma].\",\"authors\":\"Takashi Shimizu\",\"doi\":\"10.3412/jsb.70.369\",\"DOIUrl\":null,\"url\":null,\"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.\",\"PeriodicalId\":19308,\"journal\":{\"name\":\"Nihon saikingaku zasshi. Japanese journal of bacteriology\",\"volume\":\"376 1\",\"pages\":\"369-74\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"16\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nihon saikingaku zasshi. Japanese journal of bacteriology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3412/jsb.70.369\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nihon saikingaku zasshi. Japanese journal of bacteriology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3412/jsb.70.369","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 16

摘要

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。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
[Pathogenic factors of mycoplasma].
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.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
[Study on biofilm formation and heterogeneity in Clostridium perfringens]. [Wakate Colosseum for Bacteriology]. [Award Lecture]. [Workshop]. [Luncheon Seminar].
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1