1991
DOI: 10.1016/0024-3205(91)90405-z
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Interleukin-1 is cytoprotective, antisecretory, stimulates PGE2 synthesis by the stomach, and retards gastric emptying

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Cited by 173 publications
(82 citation statements)
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“…In hu-man gastric fibroblasts, stimulation with IL-1␤ induces COX-2-dependent PGE 2 generation (27), leading to the expression of hepatocyte growth factor (27,28), which stimulates proliferation of rabbit gastric epithelial cells (28,29). Furthermore, cytoprotection by IL-1␤ against ethanol-induced gastric injury was shown to be dependent on the generation of PGE 2 in an animal model (30). Consequently, it is conceivable that TGF-␣ and IL-1␤ are implicated in the healing of gastric lesions through, at least in part, COX-2-dependent PGE 2 generation.…”
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confidence: 97%
“…In hu-man gastric fibroblasts, stimulation with IL-1␤ induces COX-2-dependent PGE 2 generation (27), leading to the expression of hepatocyte growth factor (27,28), which stimulates proliferation of rabbit gastric epithelial cells (28,29). Furthermore, cytoprotection by IL-1␤ against ethanol-induced gastric injury was shown to be dependent on the generation of PGE 2 in an animal model (30). Consequently, it is conceivable that TGF-␣ and IL-1␤ are implicated in the healing of gastric lesions through, at least in part, COX-2-dependent PGE 2 generation.…”
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confidence: 97%
“…PGE 2 is synthesised in gastric glands and its synthesis is enhanced by many factors such as cytokines (Robert et al 1991) or cGMP via NO (Uno et al 1997). PGE 2 has been proposed as a key mediator of mucosal defence.…”
Section: Figure 10mentioning
confidence: 99%
“…On the other hand, prostaglandin E 2 (PGE 2 ) is generally known to be a local chemical mediator that protects the gastric mucosa from acid-peptic injury. PGE 2 synthesis is reported to be stimulated in gastric mucous cells in the presence of biologically active substances, such as cytokines, nitric oxide (NO) and ACh (Robert et al 1991;Uno et al 1997). McQueen et al (1983) reported that prostaglandins could increase the thickness of the mucosal gel layer.…”
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confidence: 99%
“…To facilitate evaluation of enzyme compositions, formulations, and dosing regimens, we sought to develop a rodent model for gluten digestion. A number of studies (Robert et al, 1991;Matsuda et al, 1993;Burton-Freeman et al, 1997;Izbeki et al, 2001;Overhaus et al, 2004;Turan and Ozdemir, 2004) have exploited the intrinsic similarities between gastrointestinal metabolism of food in rats and hu-mans. Rats may be an effective model for gluten digestion because they are able to eat and digest a significant level of food (on the order of several grams, which would represent a physiological gluten load for a Celiac patient) in a suitable time frame (i.e., in approximately 5-8 h) (Kaneko et al, 1995).…”
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confidence: 99%