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吲哚信号传导可减少单核细胞增生李斯特菌的生物膜形成及相关毒力。

Indole signaling decreases biofilm formation and related virulence of Listeria monocytogenes.

作者信息

Rattanaphan Paramaporn, Mittraparp-Arthorn Pimonsri, Srinoun Kanitta, Vuddhakul Varaporn, Tansila Natta

机构信息

Department of Microbiology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90110, Thailand.

Faculty of Medical Technology, Prince of Songkla University, Hat Yai, Songkhla 90110, Thailand.

出版信息

FEMS Microbiol Lett. 2020 Jul 1;367(14). doi: 10.1093/femsle/fnaa116.

DOI:10.1093/femsle/fnaa116
PMID:32658271
Abstract

Bacterial communication system known as quorum sensing (QS) is a pivotal system for bacterial survival, adaptation and pathogenesis. Members in the multicellular community may synthesize or acquire a signaling molecule in order to elicit downstream cellular processes. Roles of indole and derivatives, a new class of quorum-sensing signal molecules, in various bacterial physiologies and virulence have been reported recently. Indole is normally found in mammal gastrointestinal tract as a metabolite of tryptophan metabolism by microbiota. Therefore, interspecies connection via indole signaling among commensal bacteria and enteric pathogens could be anticipated. Effects of indole exposure on the virulence of Listeria monocytogenes were investigated by phenotypic and molecular approaches. Results demonstrated that synthetic indole and indole-rich conditioned medium significantly diminished biofilm formation and related virulence of L. monocytogenes including motility, cell aggregation and exopolysaccharide production. Transcript levels of virulence-associated (pssE, dltA, flaA, fliI, motB, agrA and hly) and regulatory genes (codY, sigB, prfA and gmaR) were substantially downregulated in indole-treated cells. Only mogR gene encoding for a repressor of motility genes was upregulated after indole exposure. Our findings raise the possibility that L. monocytogenes may acquire indole signaling from gut microbiota for resource-effective adaptation upon transition to new environment.

摘要

被称为群体感应(QS)的细菌通讯系统是细菌生存、适应和致病的关键系统。多细胞群落中的成员可能会合成或获取一种信号分子,以引发下游的细胞过程。最近有报道称,一类新型群体感应信号分子——吲哚及其衍生物在各种细菌生理和毒力中发挥作用。吲哚通常作为微生物群对色氨酸代谢的一种代谢产物存在于哺乳动物胃肠道中。因此,可以预期共生细菌和肠道病原体之间会通过吲哚信号进行种间联系。通过表型和分子方法研究了吲哚暴露对单核细胞增生李斯特菌毒力的影响。结果表明,合成吲哚和富含吲哚的条件培养基显著减少了单核细胞增生李斯特菌的生物膜形成以及包括运动性、细胞聚集和胞外多糖产生在内的相关毒力。在吲哚处理的细胞中,毒力相关基因(pssE、dltA、flaA、fliI、motB、agrA和hly)和调控基因(codY、sigB、prfA和gmaR)的转录水平大幅下调。吲哚暴露后,只有编码运动基因阻遏物的mogR基因上调。我们的研究结果提出了一种可能性,即单核细胞增生李斯特菌可能从肠道微生物群中获取吲哚信号,以便在过渡到新环境时进行资源有效适应。

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