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Interleukin-1 beta release from rat gastric fundus
P Montuschi1, G Tringali, A Mirtella
1Institute of Pharmacology, Catholic University Medical School, Rome, Italy.
The American Journal of Physiology
|August 1, 1996
Summary
Interleukin-1 beta (IL-1 beta) is released by rat gastric tissue and may protect against acid-induced injury. Glucocorticoids inhibit this release, potentially contributing to gastric damage during stress or steroid therapy.
Area of Science:
- Gastroenterology
- Immunology
- Physiology
Background:
- Interleukin-1 (IL-1) regulates gastric functions centrally and directly affects gastric motility.
- The role of local IL-1 production within the gastric tissue itself remains to be elucidated.
Purpose of the Study:
- To determine if rat gastric fundi produce and release Interleukin-1 beta (IL-1 beta) in vitro.
- To investigate factors influencing IL-1 beta release from gastric tissue.
Main Methods:
- Explants of rat gastric tissue were used to measure IL-1 beta release.
- Electrical stimulation and agents affecting IL-1 biosynthesis were applied.
- Glucocorticoids and agents reducing gastric acid secretion were tested for their effects on IL-1 beta release.
Main Results:
- Measurable amounts of IL-1 beta immunoreactivity were released from explanted rat gastric tissue.
- Electrical stimulation and IL-1 biosynthesis inducers did not affect IL-1 beta release.
- Glucocorticoids, such as dexamethasone, inhibited IL-1 beta release.
- Agents reducing gastric acid secretion also inhibited IL-1 beta release.
Conclusions:
- Rat gastric fundi produce and release IL-1 beta.
- IL-1 beta release is inhibited by glucocorticoids and agents reducing gastric acid secretion.
- IL-1 beta release may be stimulated by gastric acid, acting as a protective mechanism against acid-induced mucosal injury.
- Glucocorticoid inhibition of IL-1 beta release might be implicated in the pathogenesis of gastric damage during stress or steroid therapy.