Molecular Characterization of Virulence Factors in Enterotoxigenic Escherichia coli

Document Type: Review Article

Authors

1 Young Researchers and Elite Club, Andimeshk Branch, Islamic Azad University, Andimeshk, Iran

2 Department of Biology, Faculty of Sciences, shahed University, Tehran, Iran

3 Department of Biology, Faculty of Science, Imam-Hossein University, Tehran, Iran

4 Education Development Center, School of Medical, Medical University of Shiraz, Shiraz, Iran

Abstract

Millions of diarrheal disease is made by Enterotoxigenic E. coli (ETEC) each year, specifically in developing countries. In the pathogenesis of ETEC infections, the first phase is sticking of the bacterium to the minute intestinal epithelium, as a result of colonization factors (CFs) mediation and subsequently generate enterotoxins. These CFs in accordance with their structure are diverged into discrete groups. CFA/I and CS6 are two of the most typical CFs. CFA/I is a fimbriae consists of a superior subunit, CfaB and inferior subunit, CfaE. CS6 is non-fimbrial which includes two main subunits, CssA and CssB. The enterotoxins caused by ETEC are related to two eminent classes of heat-labile toxins (LT) and heat stable toxins (ST). LT is formed of five B subunits and a single enzymatically active A. Its B subunits tied up to the enteral GM1 ganglioside receptors in the intestinal epithelium and A subunit whose ADP-ribosylating activity culminates in cellular adenylcyclase activation and an increase in cAMP, efflux of chloride ions and water and succeeding watery diarrhea. Guanylatecyclase (GC) is receptor for the ST toxin. Intracellular levels of cyclic guanosine monophosphate (cGMP) increase when ST binds to GC. Such increase in cGMP permits activation of cystic fibrosis transmembrane conductance regulator (CFTR) by phosphorylation-dependent cGMP protein kinase II producing an escalation in salt and secretion of water and prevention of sodium absorption through h the apical Na/H channel.More information about the CFs and enterotoxins of pathogen leads to more founding of ETEC virulence, and the founding is important to designing an appropriate vaccine.

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