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Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
Human rotavirus enteritis induced in conventional piglets. Intestinal structure and transport
The Journal of Clinical Investigation
|December 1, 1977
Summary
Infantile rotavirus infection impairs glucose-coupled sodium transport in the jejunum, altering villus enterocyte enzyme activity. This occurs even when viral presence is minimal, mimicking other invasive enteritis forms.
Area of Science:
- Gastroenterology
- Virology
- Molecular Biology
Background:
- Infantile viral gastroenteritis poses a significant health challenge.
- Understanding rotavirus pathogenesis is crucial for effective treatment.
Purpose of the Study:
- To investigate the effects of rotavirus infection on jejunal ion transport and enterocyte function in piglets.
- To elucidate the mechanisms underlying rotavirus-induced gastroenteritis.
Main Methods:
- Studied Na+ and Cl- fluxes in vitro in jejunal epithelium of rotavirus-infected and control piglets.
- Assessed intestinal morphology, viral antigen presence, and enzyme activities (thymidine kinase, sucrase) in enterocytes.
Main Results:
- Rotavirus infection led to shorter villi and deeper crypts in the jejunum.
- Glucose-coupled Na+ transport response was blunted in infected piglets.
- Increased thymidine kinase and decreased sucrase activity were observed in enterocytes of infected piglets.
Conclusions:
- Rotavirus infection impairs glucose-coupled Na+ transport in the jejunum.
- Jejunal villus epithelium exhibits crypt-like enzyme characteristics post-infection.
- Findings are consistent with invasive enteritis and distinct from enterotoxigenic diarrhea.
