Enterotoxigenic Escherichia coli: intestinal pathogenesis mechanisms and colonization resistance by gut microbiota

Gut Microbes. 2022 Jan-Dec;14(1):2055943. doi: 10.1080/19490976.2022.2055943.


Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhea in children and travelers in developing countries. ETEC is characterized by the ability to produce major virulence factors including colonization factors (CFs) and enterotoxins, that bind to specific receptors on epithelial cells and induce diarrhea. The gut microbiota is a stable and sophisticated ecosystem that performs a range of beneficial functions for the host, including protection against pathogen colonization. Understanding the pathogenic mechanisms of ETEC and the interaction between the gut microbiota and ETEC represents not only a research need but also an opportunity and challenge to develop precautions for ETEC infection. Herein, this review focuses on recent discoveries about ETEC etiology, pathogenesis and clinical manifestation, and discusses the colonization resistances mediated by gut microbiota, as well as preventative strategies against ETEC with an aim to provide novel insights that can reduce the adverse effect on human health.

Keywords: Enterotoxigenic Escherichia coli; colonization resistance; enterotoxin; gut microbiota; pathogenesis.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Child
  • Ecosystem
  • Enterotoxigenic Escherichia coli*
  • Escherichia coli Infections* / prevention & control
  • Gastrointestinal Microbiome*
  • Humans
  • Intestines

Grants and funding

This study was supported by the National Natural Science Foundation of China (31930106, 31829004, and 31722054), the National Ten-thousand Talents Program of China (23070201), the Henan Province Public Benefit Research Foundation (201300111200-05), the 2115 Talent Development Program of China Agricultural University (1041-00109019), the Developmental Fund by Henan Wofengde Biological Technology Co., Ltd. (201905410411435), and the 111 Project (B16044).