BACKGROUND: In a previous study we showed that interleukin 1beta (IL-1beta) caused recurrence of gastric ulcers in rats, and that adhesion molecules (intercellular adhesion molecule 1 and leucocytic beta2 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-1beta, 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 microg/kg IL-1beta intraperitoneally. Another group of rats was given 20 mg/kg omeprazole for three days to inhibit acid secretion, and received IL-1beta 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-1beta treatment. Some rats were given acid alone at the same time points. Expression of adhesion molecules was examined immunohistochemically and concentrations of IL-1beta and tumour necrosis factor alpha (TNF-alpha) were measured by ELISA in scar tissue 24 hours after IL-1beta treatment. RESULTS: IL-1beta increased expression of adhesion molecules and concentrations of IL-1beta and TNF-alpha in scar tissue by 24 hours after IL-1beta treatment, and nine of 11 healed ulcers had recurred by 48 hours. Omeprazole inhibited the effects of IL-1beta. 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-1beta, and gastric acid stimulates the inflammatory process in scarred mucosa during ulcer recurrence.
BACKGROUND: In a previous study we showed that interleukin 1beta (IL-1beta) caused recurrence of gastric ulcers in rats, and that adhesion molecules (intercellular adhesion molecule 1 and leucocytic beta2 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-1beta, 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 microg/kg IL-1beta intraperitoneally. Another group of rats was given 20 mg/kg omeprazole for three days to inhibit acid secretion, and received IL-1beta 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-1beta treatment. Some rats were given acid alone at the same time points. Expression of adhesion molecules was examined immunohistochemically and concentrations of IL-1beta and tumour necrosis factor alpha (TNF-alpha) were measured by ELISA in scar tissue 24 hours after IL-1beta treatment. RESULTS:IL-1beta increased expression of adhesion molecules and concentrations of IL-1beta and TNF-alpha in scar tissue by 24 hours after IL-1beta treatment, and nine of 11 healed ulcers had recurred by 48 hours. Omeprazole inhibited the effects of IL-1beta. 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-1beta, and gastric acid stimulates the inflammatory process in scarred mucosa during ulcer recurrence.
Authors: T Hayakawa; Y Fujiwara; M Hamaguchi; T Sugawa; M Okuyama; E Sasaki; T Watanabe; K Tominaga; N Oshitani; K Higuchi; T Arakawa Journal: Gut Date: 2005-10-06 Impact factor: 23.059
Authors: Mohamed M Elseweidy; Nahla N Younis; Rawia S Amin; Fatma R Abdallah; Azza M Fathy; Zeinab A Yousif Journal: Dig Dis Sci Date: 2008-03-27 Impact factor: 3.199