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Eradication of Helicobacter pylori and resolution of gastritis in the gastric mucosa of IL-10-deficient mice.
Helicobacter 2005; 10(5):407-15H

Abstract

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+Show Affiliations

Department of Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

16181351

Citation

Matsumoto, Yuko, et al. "Eradication of Helicobacter Pylori and Resolution of Gastritis in the Gastric Mucosa of IL-10-deficient Mice." Helicobacter, vol. 10, no. 5, 2005, pp. 407-15.
Matsumoto Y, Blanchard TG, Drakes ML, et al. Eradication of Helicobacter pylori and resolution of gastritis in the gastric mucosa of IL-10-deficient mice. Helicobacter. 2005;10(5):407-15.
Matsumoto, Y., Blanchard, T. G., Drakes, M. L., Basu, M., Redline, R. W., Levine, A. D., & Czinn, S. J. (2005). Eradication of Helicobacter pylori and resolution of gastritis in the gastric mucosa of IL-10-deficient mice. Helicobacter, 10(5), pp. 407-15.
Matsumoto Y, et al. Eradication of Helicobacter Pylori and Resolution of Gastritis in the Gastric Mucosa of IL-10-deficient Mice. Helicobacter. 2005;10(5):407-15. PubMed PMID: 16181351.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Eradication of Helicobacter pylori and resolution of gastritis in the gastric mucosa of IL-10-deficient mice. AU - Matsumoto,Yuko, AU - Blanchard,Thomas G, AU - Drakes,Maureen L, AU - Basu,Malini, AU - Redline,Raymond W, AU - Levine,Alan D, AU - Czinn,Steven J, PY - 2005/9/27/pubmed PY - 2005/11/16/medline PY - 2005/9/27/entrez SP - 407 EP - 15 JF - Helicobacter JO - Helicobacter VL - 10 IS - 5 N2 - 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. SN - 1083-4389 UR - https://www.unboundmedicine.com/medline/citation/16181351/Eradication_of_Helicobacter_pylori_and_resolution_of_gastritis_in_the_gastric_mucosa_of_IL_10_deficient_mice_ L2 - https://doi.org/10.1111/j.1523-5378.2005.00349.x DB - PRIME DP - Unbound Medicine ER -