Abstract
Enterotoxigenic Escherichia coli (ETEC) produces the heat-stable enterotoxin b (STb), which is responsible for secretory diarrhea in humans and animals. This toxin is secreted within the intestinal lumen of animals and humans following ETEC colonization, becoming active on enterocytes and altering fluid homeostasis. Several studies have outlined the nature of this toxin and its effects on gut health and the integrity of the intestinal epithelium. This review summarizes the mechanisms of how STb alters the gastrointestinal tract. These include the manipulation of mucosal tight junction protein integrity, the formation of enterocyte cellular pores and toxin internalization and the stimulation of programmed cell death. We conclude with insights into the potential link between STb intoxication and altered gut hormone regulation, and downstream physiology.
Highlights
Infectious diarrhea is one of the leading causes of death in children of developing countries [1].Enterotoxigenic Escherichia coli (ETEC) is known to cause travelers’ diarrhea and diarrhea in farm animals [2]
Key Contribution: We summarize gastrointestinal related alterations caused by the ETEC stable enterotoxin b (STb) toxin and the potential fate of gut hormone regulation
All of these combined the junctions (TJs) alterations during an ETEC infection by the STb toxin are involved with disrupting intestinal barrier function, impairing paracellular flux mechanisms and increasing the permeability of the epithelium
Summary
Infectious diarrhea is one of the leading causes of death in children of developing countries [1]. The heat-stable enterotoxin b (STb) is one of several toxins secreted by ETEC responsible for inducing diarrhea [9]. The internalization of STb by the cells results in the to activation of of a a pertussis toxin-sensitive regulatory protein (Gαi). This leads an influx pertussis toxin-sensitive protein (Gαi3) This leads to an influx of extracellular calcium ionsGTP-binding into the cell regulatory by means of a receptor-dependent ligand-gated calcium extracellular ions into the cell by calcium means of a receptor-dependent ligand-gated channel [15]. Are many This gut functions can become alteredanimals, by the STb toxinas during an an ETEC toxin haswhich been observed to negatively effect numerous as well humans.
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