BACKGROUND: Helicobacter pylori has been shown to induce pronounced gastric inflammation in the absence of interleukin-10 (IL-10) by 6 weeks post inoculation. The ability of IL-10(-/-) mice to eradicate H. pylori has not been demonstrated, possibly due to early sacrifice. Therefore, the long-term effect of enhanced gastritis on H. pylori colonization was determined in IL-10(-/-) mice. METHODS: C57BL/6 and IL-10(-/-) mice were infected with H. pylori and assessed for the degree of gastritis, bacterial load, and in vitro T-cell recall response at 4 and 16 weeks of infection. RESULTS: Infection of IL-10(-/-) mice resulted in significantly more severe gastritis than wild-type control mice and eradication of H. pylori by 4 weeks post inoculation. By 16 weeks, the level of gastritis in IL-10(-/-) was reduced to the levels observed in wild-type mice. Splenocytes from IL-10(-/-) mice were prone to produce significantly greater amounts of IFN-gamma than wild-type mice when stimulated with bacterial antigens. CONCLUSIONS: These results indicate that the host is capable of spontaneously eradicating H. pylori from the gastric mucosa when inflammation is elevated beyond the chronic inflammation induced in wild-type mice, and that the gastritis dissipates following bacterial eradication. Additionally, these data provide support for a model of gastrointestinal immunity in which naturally occurring IL-10-producing regulatory T cells modulate the host response to gastrointestinal bacteria.
BACKGROUND:Helicobacter pylori has been shown to induce pronounced gastric inflammation in the absence of interleukin-10 (IL-10) by 6 weeks post inoculation. The ability of IL-10(-/-) mice to eradicate H. pylori has not been demonstrated, possibly due to early sacrifice. Therefore, the long-term effect of enhanced gastritis on H. pylori colonization was determined in IL-10(-/-) mice. METHODS: C57BL/6 and IL-10(-/-) mice were infected with H. pylori and assessed for the degree of gastritis, bacterial load, and in vitro T-cell recall response at 4 and 16 weeks of infection. RESULTS:Infection of IL-10(-/-) mice resulted in significantly more severe gastritis than wild-type control mice and eradication of H. pylori by 4 weeks post inoculation. By 16 weeks, the level of gastritis in IL-10(-/-) was reduced to the levels observed in wild-type mice. Splenocytes from IL-10(-/-) mice were prone to produce significantly greater amounts of IFN-gamma than wild-type mice when stimulated with bacterial antigens. CONCLUSIONS: These results indicate that the host is capable of spontaneously eradicating H. pylori from the gastric mucosa when inflammation is elevated beyond the chronic inflammation induced in wild-type mice, and that the gastritis dissipates following bacterial eradication. Additionally, these data provide support for a model of gastrointestinal immunity in which naturally occurring IL-10-producing regulatory T cells modulate the host response to gastrointestinal bacteria.
Authors: Nuruddeen D Lewis; Mohammad Asim; Daniel P Barry; Thibaut de Sablet; Kshipra Singh; M Blanca Piazuelo; Alain P Gobert; Rupesh Chaturvedi; Keith T Wilson Journal: J Immunol Date: 2011-02-04 Impact factor: 5.422
Authors: Elizabeth S DeLyria; John G Nedrud; Peter B Ernst; Mohammad S Alam; Raymond W Redline; Hua Ding; Steven J Czinn; Jinghua Xu; Thomas G Blanchard Journal: Helicobacter Date: 2011-06 Impact factor: 5.753
Authors: Chung-Wei Lee; Varada P Rao; Arlin B Rogers; Zhongming Ge; Susan E Erdman; Mark T Whary; James G Fox Journal: Infect Immun Date: 2007-03-12 Impact factor: 3.441
Authors: Peter Mitchell; Conrad Germain; Pier Luigi Fiori; Wafa Khamri; Graham R Foster; Subrata Ghosh; Robert I Lechler; Kathleen B Bamford; Giovanna Lombardi Journal: Infect Immun Date: 2006-11-13 Impact factor: 3.441
Authors: Yu Qiao; Brian M Gray; Mohammed H Sofi; Laura D Bauler; Kathryn A Eaton; Mary X D O'Riordan; Cheong-Hee Chang Journal: Open J Immunol Date: 2011-12-30