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The bile salt glycocholate induces global changes in gene and protein expression and activates virulence in enterotoxigenic Escherichia coli

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机构: [1]Department of Microbiology, Tumor and Cell biology, Karolinska Institutet, Stockholm, Box 280, S-17177, Stockholm, Sweden. [2]Institute of Biomedicine, Department of Microbiology and Immunology, University of Gothenburg, Box 435, S-405 30, Göteborg, Sweden. [3]CAS Key Laboratory of Pathogenic Microbiology & Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China. [4]Department of Biomedical Informatics, College of Medicine, The University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA. [5]Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China. [6]Department of Pathogenic Biology, School of Basic Medical Sciences, Southwest Medical University, Zhongshan Road, Luzhou, Sichuan, China.
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Pathogenic bacteria use specific host factors to modulate virulence and stress responses during infection. We found previously that the host factor bile and the bile component glyco-conjugated cholate (NaGCH, sodium glycocholate) upregulate the colonization factor CS5 in enterotoxigenic Escherichia coli (ETEC). To further understand the global regulatory effects of bile and NaGCH, we performed Illumina RNA-Seq and found that crude bile and NaGCH altered the expression of 61 genes in CS5 + CS6 ETEC isolates. The most striking finding was high induction of the CS5 operon (csfA-F), its putative transcription factor csvR, and the putative ETEC virulence factor cexE. iTRAQ-coupled LC-MS/MS proteomic analyses verified induction of the plasmid-borne virulence proteins CS5 and CexE and also showed that NaGCH affected the expression of bacterial membrane proteins. Furthermore, NaGCH induced bacteria to aggregate, increased their adherence to epithelial cells, and reduced their motility. Our results indicate that CS5 + CS6 ETEC use NaGCH present in the small intestine as a signal to initiate colonization of the epithelium.

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大类 | 3 区 综合性期刊
小类 | 3 区 综合性期刊
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大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
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Q1 MULTIDISCIPLINARY SCIENCES
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Q1 MULTIDISCIPLINARY SCIENCES

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第一作者机构: [1]Department of Microbiology, Tumor and Cell biology, Karolinska Institutet, Stockholm, Box 280, S-17177, Stockholm, Sweden.
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