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Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice.

Publication ,  Journal Article
Hale, LP; Perera, D; Gottfried, MR; Maggio-Price, L; Srinivasan, S; Marchuk, D
Published in: Helicobacter
December 2007

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 approximately 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.

Duke Scholars

Published In

Helicobacter

DOI

ISSN

1083-4389

Publication Date

December 2007

Volume

12

Issue

6

Start / End Page

598 / 604

Location

England

Related Subject Headings

  • Mutation
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Intracellular Signaling Peptides and Proteins
  • Interleukin-10
  • Inflammatory Bowel Diseases
  • Helicobacter Infections
  • Genetic Predisposition to Disease
  • Gastroenterology & Hepatology
 

Citation

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Hale, L. P., Perera, D., Gottfried, M. R., Maggio-Price, L., Srinivasan, S., & Marchuk, D. (2007). Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice. Helicobacter, 12(6), 598–604. https://doi.org/10.1111/j.1523-5378.2007.00552.x
Hale, Laura P., Dinushi Perera, Marcia R. Gottfried, Lillian Maggio-Price, Sudha Srinivasan, and Douglas Marchuk. “Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice.Helicobacter 12, no. 6 (December 2007): 598–604. https://doi.org/10.1111/j.1523-5378.2007.00552.x.
Hale LP, Perera D, Gottfried MR, Maggio-Price L, Srinivasan S, Marchuk D. Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice. Helicobacter. 2007 Dec;12(6):598–604.
Hale, Laura P., et al. “Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice.Helicobacter, vol. 12, no. 6, Dec. 2007, pp. 598–604. Pubmed, doi:10.1111/j.1523-5378.2007.00552.x.
Hale LP, Perera D, Gottfried MR, Maggio-Price L, Srinivasan S, Marchuk D. Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice. Helicobacter. 2007 Dec;12(6):598–604.
Journal cover image

Published In

Helicobacter

DOI

ISSN

1083-4389

Publication Date

December 2007

Volume

12

Issue

6

Start / End Page

598 / 604

Location

England

Related Subject Headings

  • Mutation
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Intracellular Signaling Peptides and Proteins
  • Interleukin-10
  • Inflammatory Bowel Diseases
  • Helicobacter Infections
  • Genetic Predisposition to Disease
  • Gastroenterology & Hepatology