RT Journal Article
SR Electronic
T1 Acid regulates inflammatory response in a rat model of induction of gastric ulcer recurrence by interleukin 1β
JF Gut
JO Gut
FD BMJ Publishing Group Ltd and British Society of Gastroenterology
SP 774
OP 781
DO 10.1136/gut.48.6.774
VO 48
IS 6
A1 T Watanabe
A1 K Higuchi
A1 K Tominaga
A1 Y Fujiwara
A1 T Arakawa
YR 2001
UL http://gut.bmj.com/content/48/6/774.abstract
AB BACKGROUND In a previous study we showed that interleukin 1β (IL-1β) caused recurrence of gastric ulcers in rats, and that adhesion molecules (intercellular adhesion molecule 1 and leucocytic β2 integrins) play a role in this recurrence. Although gastric acid plays an important role in many types of gastric injuries, including peptic ulcer recurrence, the mechanism(s) remains unclear.AIMS To examine the involvement of gastric acid in induction of ulcer recurrence by IL-1β, and to investigate the role of gastric acid in inflammatory responses during ulcer recurrence.METHODS Rats with healed ulcers were used. Rats were given 1 μg/kg IL-1β intraperitoneally. Another group of rats was given 20 mg/kg omeprazole for three days to inhibit acid secretion, and received IL-1β 20 hours after the first administration of omeprazole. They were then given 0.15 N HCl or vehicle at 0, 12, 24, and 36 hours after IL-1β treatment. Some rats were given acid alone at the same time points. Expression of adhesion molecules was examined immunohistochemically and concentrations of IL-1β and tumour necrosis factor α (TNF-α) were measured by ELISA in scar tissue 24 hours after IL-1β treatment.RESULTS IL-1β increased expression of adhesion molecules and concentrations of IL-1β and TNF-α in scar tissue by 24 hours after IL-1β treatment, and nine of 11 healed ulcers had recurred by 48 hours. Omeprazole inhibited the effects of IL-1β. HCl acid abolished the inhibitory effects of omeprazole. Acid alone affected neither expression of adhesion molecules nor cytokine concentrations, and did not cause recurrence.CONCLUSIONS Gastric acid is required for recurrence of gastric ulcers caused by IL-1β, and gastric acid stimulates the inflammatory process in scarred mucosa during ulcer recurrence.ILinterleukinTNFtumour necrosis factorICAM-1intercellular adhesion molecule 1LFA-1lymphocyte function associated antigen 1PPIproton pump inhibitor