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启动子中的单个碱基变化导致猪源鼠伤寒沙门氏菌生物膜增强。

A Single Base Change in the Promoter Resulted in Enhanced Biofilm in Swine-Derived Typhimurium.

作者信息

Li Zhe, Zhang Mengke, Lei Gaopeng, Lu Xin, Yang Xiaorong, Kan Biao

机构信息

National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 102206, China.

School of Light Industry, Beijing Technology and Business University, Beijing 100048, China.

出版信息

Microorganisms. 2024 Jun 21;12(7):1258. doi: 10.3390/microorganisms12071258.

DOI:10.3390/microorganisms12071258
PMID:39065026
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11278976/
Abstract

Pathogenic strains causing gastroenteritis typically can colonize and proliferate in the intestines of multiple host species. They retain the ability to form red dry and rough () biofilms, as seen in serovar Typhimurium. Conversely, serovar like Typhi, which can cause systemic infections and exhibit host restriction, are -negative. In this study, duck-derived strains and swine-derived strains of . Typhimurium locate on independent phylogenetic clades and display relative genomic specificity. The duck isolates appear more closely related to human blood isolates and invasive non-typhoidal (iNTS), whereas the swine isolates were more distinct. Phenotypically, compared to duck isolates, swine isolates exhibited enhanced biofilm formation that was unaffected by the temperature. The transcriptomic analysis revealed the upregulation of transcription as the direct cause. This upregulation may be mainly attributed to the enhanced promoter activity caused by the G-to-T substitution at position -44 of the promoter. Swine isolates have created biofilm polymorphisms by altering a conserved base present in Typhi, iNTS, and most Typhimurium (such as duck isolates). This provides a genomic characteristics perspective for understanding transmission cycles and evolution.

摘要

引起肠胃炎的致病菌株通常能够在多种宿主物种的肠道中定殖和增殖。它们保留了形成红色干燥粗糙()生物膜的能力,如鼠伤寒血清型所见。相反,能引起全身感染并表现出宿主限制的伤寒血清型则为阴性。在本研究中,鼠伤寒沙门氏菌的鸭源菌株和猪源菌株位于独立的系统发育分支上,并表现出相对的基因组特异性。鸭分离株似乎与人类血液分离株和侵袭性非伤寒(iNTS)更密切相关,而猪分离株则更具独特性。在表型上,与鸭分离株相比,猪分离株表现出增强的生物膜形成能力,且不受温度影响。转录组分析揭示了转录上调是直接原因。这种上调可能主要归因于启动子-44位的G到T替换导致的启动子活性增强。猪分离株通过改变伤寒沙门氏菌、iNTS和大多数鼠伤寒沙门氏菌(如鸭分离株)中存在的一个保守碱基,产生了生物膜多态性。这为理解传播周期和进化提供了基因组特征视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/0f1632fc24cf/microorganisms-12-01258-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/d7ce3297c8e0/microorganisms-12-01258-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/23a07d1f9239/microorganisms-12-01258-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/b7ffa76725c2/microorganisms-12-01258-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/0d2f309ba987/microorganisms-12-01258-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/b69c739e7a00/microorganisms-12-01258-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/0f1632fc24cf/microorganisms-12-01258-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/d7ce3297c8e0/microorganisms-12-01258-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/23a07d1f9239/microorganisms-12-01258-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/b7ffa76725c2/microorganisms-12-01258-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/0d2f309ba987/microorganisms-12-01258-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/b69c739e7a00/microorganisms-12-01258-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d5/11278976/0f1632fc24cf/microorganisms-12-01258-g006.jpg

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