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Updated: Sep 26, 2026

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages
09:39

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages

Published on: May 30, 2013

Development of microbial-human enterocyte interaction: cholera toxin

Lei Lu1, Manuel E Baldeon, Tor Savidge

  • 1Combined Program in Pediatric Gastroenterology and Nutrition, Harvard Medical School, Director, Developmental Gastroenterology Laboratory, Massachusetts General Hospital, 114 16th Street (114-3503), Charlestown, MA 02129-4404, U.S.A.

Pediatric Research
|May 9, 2003
PubMed

Insights

Infant diarrhea is a global health risk. This study shows immature human intestines are more susceptible to cholera toxin due to developmental changes, impacting infant infectious disease strategies.

Area of Science:

  • Gastroenterology
  • Pediatric Infectious Diseases
  • Developmental Biology

Background:

  • Diarrhea poses a significant global health threat to infants and children.
  • Neonatal period presents increased severity and incidence of certain toxigenic diarrheas.
  • Previous research indicated developmental differences in cholera toxin-induced secretion in animal models.

Purpose of the Study:

  • To investigate the role of human intestinal development in cholera toxin-induced secretion.
  • To determine if developmental up-regulation of signaling pathways contributes to enhanced susceptibility in immature intestines.

Main Methods:

  • Utilized experimental models of human intestinal development, including fetal cell lines.
  • Employed a micro-Ussing chamber for physiological measurements.
  • Incorporated organ cultures and fetal intestinal xenograft transplants for comprehensive analysis.

Main Results:

  • Provided preliminary evidence of enhanced cholera toxin secretion in immature human small intestine.
  • Indicated a developmental up-regulation of the cyclic adenosine monophosphate (cAMP) response in immature intestines.
  • Identified potential up-regulation of postreceptor signal transduction molecules.

Conclusions:

  • Immature human small intestine exhibits an enhanced secretory response to cholera toxin, partly due to developmental up-regulation of the cAMP pathway.
  • Further research is necessary to elucidate other developmental factors, such as receptor expression.
  • Findings may inform strategies for preventing and treating infant cholera and other age-related intestinal infections.

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