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智胜宿主:细菌操纵免疫反应以利于其生存。

Out-Smarting the Host: Bacteria Maneuvering the Immune Response to Favor Their Survival.

机构信息

Department of Medicine, National Jewish Health, Denver, CO, United States.

出版信息

Front Immunol. 2020 May 12;11:819. doi: 10.3389/fimmu.2020.00819. eCollection 2020.

DOI:10.3389/fimmu.2020.00819
PMID:32477341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7235365/
Abstract

Bacteria adapt themselves to various environmental conditions in nature, which can lead to bacterial adaptation and persistence in the host as commensals or pathogens. In healthy individuals, host defense mechanisms prevent the opportunistic bacteria/commensals from becoming a pathological infection. However, certain pathological conditions can impair normal defense barriers leading to bacterial survival and persistence. Under pathological conditions such as chronic lung inflammation, bacteria employ various mechanisms from structural changes to protease secretion to manipulate and evade the host immune response and create a niche permitting commensal bacteria to thrive into infections. Therefore, understanding the mechanisms by which pathogenic bacteria survive in the host tissues and organs may offer new strategies to overcome persistent bacterial infections. In this review, we will discuss and highlight the complex interactions between airway pathogenic bacteria and immune responses in several major chronic inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD).

摘要

细菌在自然界中适应各种环境条件,这可能导致细菌作为共生菌或病原体在宿主中适应和持续存在。在健康个体中,宿主防御机制可防止机会性细菌/共生菌发展为病理性感染。然而,某些病理条件会损害正常的防御屏障,导致细菌存活和持续存在。在慢性肺部炎症等病理条件下,细菌会利用各种机制,包括结构改变和蛋白酶分泌,来操纵和逃避宿主的免疫反应,并创造一个小生境,使共生菌能够茁壮成长为感染。因此,了解致病性细菌在宿主组织和器官中存活的机制可能为克服持续性细菌感染提供新的策略。在这篇综述中,我们将讨论和强调气道致病菌与哮喘和慢性阻塞性肺疾病(COPD)等几种主要慢性炎症性疾病中的免疫反应之间的复杂相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7580/7235365/fb375b08ab90/fimmu-11-00819-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7580/7235365/fb375b08ab90/fimmu-11-00819-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7580/7235365/fb375b08ab90/fimmu-11-00819-g001.jpg

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Nontuberculous Mycobacterial Infections in Cystic Fibrosis.囊性纤维化中的非结核分枝杆菌感染
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The E3 Ubiquitin Protein Ligase LINCR Amplifies the TLR-Mediated Signals through Direct Degradation of MKP1.E3 泛素蛋白连接酶 LINCR 通过直接降解 MKP1 来放大 TLR 介导的信号。
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