ArcA positively regulates the expression of virulence genes and contributes to virulence of porcine Shiga toxin-producing enterotoxigenic Escherichia coli

文献类型： 外文期刊

第一作者： Jiang, Fengwei

作者： Jiang, Fengwei;Yang, Yan;Mao, Zhao;Cai, Wentong;Li, Ganwu;Jiang, Fengwei;Li, Ganwu

作者机构：

关键词： Shiga toxin-producing enterotoxigenic Escherichia coli (STEC/ETEC); ArcA; virulence regulation; attenuation; virulence factor

期刊名称：MICROBIOLOGY SPECTRUM （ 影响因子：3.7； 五年影响因子：5.9 ）

ISSN： 2165-0497

年卷期： 2023 年

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收录情况： SCI

摘要： Enterotoxigenic Escherichia coli (ETEC) cause severe diarrhea in humans and animals. These bacteria encode two major classes of virulence factors, adhesins that promote colonization of the small intestine and enterotoxins that induce fluid secretion and thus diarrhea. Oxygen and redox sensors are regulators of virulence expression in multiple bacterial pathogens. In this study, we show that microaerobic conditions enhance the expression of virulence factors in a porcine Shiga toxin-producing ETEC (STEC/ETEC) strain. We then investigated the role of the aerobic respiration control regulator ArcA in the pathogenicity and virulence regulation in STEC/ETEC. In a mouse model, deletion of arcA caused less severe pathology, and the arcA mutant displayed lower levels of colonization and obvious weight gain of the mice compared to the wild type (WT). In a cell culture model, a lack of arcA reduced the adherence of STEC/ETEC to porcine intestinal epithelial cells. Furthermore, ArcA positively regulated the expression of several key virulence factors, including F18 fimbriae (fed), heat-labile (eltA) and heat-stable (estB) toxins, Shiga toxin 2e (stx2e), and hemolysin (hlyC), under microaerobic conditions and in vivo conditions. We then found that ArcA positively regulated the expression of eltA, estB, and hlyC by competing with a global repressor H-NS (histone-like nucleoid structuring). Mechanistically, we show that ArcA protein directly binds to the promoters of target genes, displaces H-NS silencing from the promoter and counteracts H-NS's repression. Collectively, our data established a key role for ArcA in the pathogenicity and virulence expression of porcine STEC/ETEC.

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