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American Journal of Pathology, Vol 150, 971-979, Copyright © 1997 by American Society for Investigative Pathology

REGULAR ARTICLES

Role of neutrophils in a rat model of gastric ulcer recurrence caused by interleukin-1 beta

T Watanabe, T Arakawa, T Fukuda, K Higuchi and K Kobayashi
Third Department of Internal Medicine, Osaka City University Medical School, Japan.

The production of several cytokines such as interleukin (IL)-1 in gastric mucosa is increased in subjects infected with Helicobacter pylori, a bacterium associated with ulcer recurrence. This study was performed to determine whether the administration of IL-1 beta can cause recurrence of gastric ulcers in rats. Rats with healed ulcers received an injection of IL-1 beta (0.01 to 1 microgram/kg) or vehicle alone. Some rats received an injection of antiserum to rat neutrophils at the same time as 1 microgram/kg IL-1 beta or an injection of monoclonal antibodies against adhesion molecules (anti-intercellular adhesion molecule-1, anti-CD11a, and anti-CD11b) at 0, 12, and 24 hours after the initial injection. At this dose of IL-1 beta, the numbers of neutrophils and monocytes/macrophages infiltrating the scarred mucosa were higher at 12 and 24 hours than without injection of IL-1 beta. By 48 hours, seven of the eight bealed ulcers in the group treated with 1 microgram/kg IL-1 beta had recurred, as had one of the seven healed ulcers in the group given 0.1 microgram/kg IL-1 beta. No recurrence was found in the rats treated with 0.01 microgram/kg IL-1 beta or vehicle alone. Treatment with antiserum to neutrophils or antibodies to adhesion molecules inhibited both neutrophil infiltration into the scarred mucosa and the ulcer recurrence caused by IL-1 beta. These findings suggest possible mechanisms of recurrence of human peptic ulcers.


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Copyright © 1997 by the American Society for Investigative Pathology.