Helicobacter hepaticus promotes azoxymethane-initiated colon tumorigenesis in BALB/c-IL10-deficient mice
✍ Scribed by Claude M. Nagamine; Arlin B. Rogers; James G. Fox; David B. Schauer
- Book ID
- 102272912
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- French
- Weight
- 294 KB
- Volume
- 122
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
The BALB/c‐IL10 null mouse strain develops colitis and colitis‐associated adenocarcinomas, and is a model for idiopathic inflammatory bowel disease. We tested the hypotheses that (i) azoxymethane (AOM), a carcinogen that targets the colon, synergizes with the colonic inflammation inherent in the BALB/c‐IL10 null mouse resulting in an increase in incidence, multiplicity and/or progression of AOM‐induced tumors or colitis‐associated adenocarcinomas; and (ii) prior infection with Helicobacter hepaticus, a common enterohepatic bacterial pathogen in many research mouse colonies, increases the incidence, multiplicity and/or progression of AOM‐induced colon tumors or colitis‐associated adenocarcinomas in the BALB/c‐IL10 null mouse. We show that, within the timeframe examined, AOM‐induced colon tumors in the BALB/c‐IL10 null mouse were grossly and microscopically similar in appearance to AOM‐induced colon tumors in the wild type BALB/cJ mouse. No colitis‐associated adenocarcinomas were identified. Infection with H. hepaticus prior to AOM‐treatment also did not result in colitis‐associated adenocarcinomas but did result in a significant increase in the incidence of AOM‐induced colon tumors relative to AOM treatment alone. The AOM‐induced adenomas were predominantly exophytic and nodular or polypoid and localized to the distal colon. These results suggest that H. hepaticus promotes AOM‐induced tumorigenesis in the BALB/c‐IL10 null mouse. © 2007 Wiley‐Liss, Inc.