Abstract

Enteropathogenic E. coli (EPEC) causes acute intestinal infections in infants in the developing world. Infection typically spreads through contaminated food and water and leads to severe, watery diarrhea. EPEC attaches to the intestinal epithelial cells and directly injects virulence factors which modulate multiple signaling pathways leading to host cell dysfunction. However, the molecular mechanisms that regulate the onset of diarrhea are poorly defined. A major target of EPEC is the host cell tight junction complex which acts as a barrier and regulates the passage of water and solutes through the paracellular space. In this review, we focus on the EPEC effectors that target the epithelial barrier, alter its functions and contribute to leakage through the tight junctions.

Highlights

  • Enteropathogenic E. coli (EPEC) causes diarrhea in infants in developing countries and is a major cause of morbidity and mortality[1,2]

  • EPEC directly injects virulence factors into the host cells which target multiple signaling pathways and some have been linked to tight junction disruption[6]

  • We focus only on the EPEC effectors reported to be involved in the disruption of tight junctions

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Summary

Introduction

EPEC causes diarrhea in infants in developing countries and is a major cause of morbidity and mortality[1,2]. EPEC infection results in excessive loss of water and electrolytes from the body leading to dehydration and death[3]. The underlying molecular mechanisms are not completely understood. EPEC has been reported to disrupt the ion transporters and channels as well as tight junctions in intestinal epithelial cells leading to rapid onset of diarrhea[4,5]. EPEC directly injects virulence factors into the host cells which target multiple signaling pathways and some have been linked to tight junction disruption[6]. We focus only on the EPEC effectors reported to be involved in the disruption of tight junctions

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