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发病机制:应激适应的作用

Pathogenesis: The Role of Stress Adaptation.

作者信息

Sibanda Thulani, Buys Elna M

机构信息

Department of Consumer and Food Sciences, University of Pretoria, Private Bag X20, Hatfield, Pretoria 0028, South Africa.

Department of Applied Biology and Biochemistry, National University of Science and Technology, Bulawayo P.O. Box AC939, Zimbabwe.

出版信息

Microorganisms. 2022 Jul 27;10(8):1522. doi: 10.3390/microorganisms10081522.

Abstract

Adaptive stress tolerance responses are the driving force behind the survival ability of in different environmental niches, within foods, and ultimately, the ability to cause human infections. Although the bacterial stress adaptive responses are primarily a necessity for survival in foods and the environment, some aspects of the stress responses are linked to bacterial pathogenesis. Food stress-induced adaptive tolerance responses to acid and osmotic stresses can protect the pathogen against similar stresses in the gastrointestinal tract (GIT) and, thus, directly aid its virulence potential. Moreover, once in the GIT, the reprogramming of gene expression from the stress survival-related genes to virulence-related genes allows to switch from an avirulent to a virulent state. This transition is controlled by two overlapping and interlinked transcriptional networks for general stress response (regulated by Sigma factor B, (SigB)) and virulence (regulated by the positive regulatory factor A (PrfA)). This review explores the current knowledge on the molecular basis of the connection between stress tolerance responses and the pathogenesis of . The review gives a detailed background on the currently known mechanisms of pathogenesis and stress adaptation. Furthermore, the paper looks at the current literature and theories on the overlaps and connections between the regulatory networks for SigB and PrfA.

摘要

适应性应激耐受反应是细菌在不同环境生态位、食物中生存能力的驱动力,最终也是其引发人类感染能力的驱动力。尽管细菌应激适应性反应主要是在食物和环境中生存的必要条件,但应激反应的某些方面与细菌致病性相关。食物应激诱导的对酸和渗透压应激的适应性耐受反应可以保护病原体免受胃肠道(GIT)中类似应激的影响,从而直接有助于其毒力潜力。此外,一旦进入胃肠道,基因表达从应激存活相关基因重新编程为毒力相关基因,使细菌能够从无毒状态转变为有毒状态。这种转变由两个重叠且相互关联的转录网络控制,一个用于一般应激反应(由西格玛因子B(SigB)调节),另一个用于毒力(由正调控因子A(PrfA)调节)。本综述探讨了关于应激耐受反应与细菌致病性之间联系的分子基础的当前知识。该综述详细介绍了目前已知的发病机制和应激适应机制的背景。此外,本文还研究了关于SigB和PrfA调控网络之间重叠和联系的当前文献和理论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e35/9416357/e72185197b48/microorganisms-10-01522-g001.jpg

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