期刊
HELICOBACTER
卷 12, 期 6, 页码 598-604出版社
BLACKWELL PUBLISHING
DOI: 10.1111/j.1523-5378.2007.00552.x
关键词
inflammation; colorectal neoplasia; TGF-beta; Helicobacter; endoglin (CD105)
资金
- NCCIH NIH HHS [R21-AT002288, R21-AT002818] Funding Source: Medline
- NCI NIH HHS [R01-CA115480] Funding Source: Medline
- NHLBI NIH HHS [R01-HL49171] Funding Source: Medline
Background: Inflammatory bowel disease (IBD) is hypothesized to represent an aberrant immune response against enteric bacteria that occurs in a genetically susceptible host. Humans and mice with IBD are at markedly increased risk for colonic neoplasia. However, the long lead time required before development of inflammation-associated colon neoplasia in commonly used murine models of IBD slows the development of effective chemopreventative therapies. Materials and methods: Neonatal coinfection with Helicobacter typhlonius and Helicobacter rodentium was used to trigger the onset of IBD in mice deficient in the immunoregulatory cytokine interleukin (IL)-10. The severity of colon inflammation and incidence of neoplasia was determined histologically. Results: IL-10(-/-)mice demonstrated early onset, severe colon inflammation following neonatal infection with H. typhlonius and H. rodentium. The incidence of inflammation-associated colon neoplasia was similar to 95% at a mean age of 21 +/- 2 weeks. Mutation of endoglin, an accessory receptor for TGF-beta, did not affect the severity of IBD or the incidence of neoplasia in this model. Conclusions: The rapid onset of severe colon inflammation and multiple neoplastic lesions in the colons of IL-10(-/-) mice neonatally coinfected with H. typhlonius and H. rodentium makes this model well-suited for investigating the mechanisms involved in inflammation-associated colon cancer as well as its chemoprevention.
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