文献类型： 外文期刊

作者： Duan, Qiangde ¹ ; Pang, Shengmei ¹ ; Feng, Lili ⁴ ; Liu, Jiaqi ¹ ; Lv, Linfen ¹ ; Li, Baoliang ¹ ; Liang, Yuxuan ¹ ; Zhu, Guoqiang ¹ ;

作者机构： 1.Yangzhou Univ, Coll Vet Med, Yangzhou 225009, Jiangsu, Peoples R China

2.Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China

3.Jiangsu Joint Lab Int Cooperat Prevent & Control, Yangzhou 225009, Jiangsu, Peoples R China

4.Henan Acad Agr Sci, Inst Agr Econ & Informat, Zhengzhou 450002, Peoples R China

关键词： Heat-labile enterotoxin; ETEC; adherence; fimbriae; pathogenesis

期刊名称：VETERINARY RESEARCH （ 影响因子：3.829； 五年影响因子：4.269 ）

ISSN： 0928-4249

年卷期： 2022 年 53 卷 1 期

页码：

收录情况： SCI

摘要： As one of the crucial enterotoxins secreted by enterotoxigenic Escherichia coli (ETEC), heat-labile enterotoxin (LT) enhances bacterial adherence both in vivo and in vitro; however, the underlying mechanism remains unclear. To address this, we evaluated the adherence of LT-producing and LT-deficient ETEC strains using the IPEC-J2 cell model. The expression levels of inflammatory cytokines and chemokines, and tight-junction proteins were evaluated in IPEC-J2 cells after infection with various ETEC strains. Further, the levels of adhesins and enterotoxins were also evaluated in F4ac-producing ETEC (F4 + ETEC) strains after treatment with cyclic AMP (cAMP). The adherence of the Delta eltAB mutant was decreased compared with the wild-type strain, whereas adherence of the 1836-2/pBR322-eltAB strain was markedly increased compared with the 1836-2 parental strain. Production of LT up-regulated the expression of TNF-alpha, IL-6, CXCL-8, and IL-10 genes. However, it did not appear to affect tight junction protein expression. Importantly, we found that cAMP leads to the upregulation of adhesin production and STb enterotoxin. Moreover, the F4 + ETEC strains treated with cAMP also had greater adhesion to IPEC-J2 cells, and the adherence of Delta faeG, Delta fliC, and Delta estB mutants was decreased. These results indicate that LT enhances the adherence of F4 + ETEC due primarily to the upregulation of F4 fimbriae, flagellin, and STb enterotoxin expression and provide insights into the pathogenic mechanism of LT and ETEC.