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Published on: June 11, 2009
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Clostridium perfringens type A enterotoxin damages the rabbit colon
Jorge P Garcia1, Jihong Li, Archana Shrestha
1California Animal Health and Food Safety Laboratory System, School of Veterinary Medicine, University of California Davis, San Bernardino, California, USA.
Infection and Immunity
|March 20, 2014
Summary
Clostridium perfringens enterotoxin (CPE) causes gastrointestinal symptoms. This study shows CPE induces damage and fluid in rabbit colons, suggesting the colon plays a role in CPE-mediated diseases.
Area of Science:
- Microbiology
- Gastroenterology
- Toxicology
Background:
- Clostridium perfringens enterotoxin (CPE) is known to cause gastrointestinal symptoms.
- CPE induces fluid accumulation and tissue damage in the small intestine, but its effect on the colon is debated.
Purpose of the Study:
- To investigate the effects of CPE on rabbit colonic loops.
- To compare the effects of CPE on colonic loops with those on small intestinal loops.
- To identify the mechanisms underlying CPE-induced colonic changes.
Main Methods:
- Treatment of ligated rabbit colonic and small intestinal loops with varying concentrations of CPE.
- Administration of CPE-neutralizing monoclonal antibody, heat-inactivated CPE, antibody alone, and bovine serum albumin (BSA).
- Histological examination of tissue damage and measurement of luminal fluid accumulation.
- Western blotting to detect CPE binding, complex formation, and receptor expression (claudins-3 and -4).
Main Results:
- CPE treatment (50 or 100 μg/ml) caused significant histologic lesions and fluid accumulation in rabbit colonic loops.
- A CPE-neutralizing antibody blocked histologic damage but not fluid accumulation in colonic loops.
- Luminal fluid accumulation in colonic loops was also observed with heat-inactivated CPE, antibody alone, or BSA, suggesting osmotic contribution.
- Both small intestinal and colonic loops showed similar histologic damage and fluid accumulation after 1-hour CPE treatment.
- Western blotting confirmed CPE binding and formation of large complexes in both small intestine and colon.
- High-affinity CPE receptors, claudins-3 and -4, were detected in both organs.
Conclusions:
- CPE induces significant histologic damage and fluid accumulation in rabbit colonic loops, contrary to previous findings.
- The colon is sensitive to CPE, exhibiting similar damage and fluid accumulation as the small intestine.
- Osmolarity likely contributes to fluid accumulation in CPE-treated colonic loops.
- The presence of claudin-3 and -4 receptors in the colon supports CPE binding and potential involvement in colonic disease.
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