Febrile responses induced in adrenalectomized rats by administration of interleukin-1 beta or prostaglandin E2.

These studies utilized a sensitive and specific radioimmunoassay for interleukin 1 beta (IL-1 beta) to compare release of IL-1 by human alveolar macrophages and blood monocytes. The studies demonstrate that alveolar macrophages release amounts of antigenic IL-1 beta that are similar to that of blood monocytes. The amounts of IL-1 released were similar for both cell types at early (4 h) and late (24 h) time points and with differing amounts of stimuli [endotoxin; lipopolysaccharide (LPS)]. In addition, alveolar macrophages actually produced more total IL-1 (intracellular IL-1 plus released IL-1) than did blood monocytes. Alveolar macrophages that were stimulated with LPS released significantly more prostaglandin E2 (PGE2, an inhibitor of IL-1) than did blood monocytes. These studies demonstrate that human alveolar macrophages are not defective in their capacity to release IL-1.

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Interleukin-1 beta acts at hypothalamic sites to inhibit gastric acid secretion in rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.3.g414 ◽

1992 ◽

Vol 263 (3) ◽

pp. G414-G418 ◽

Cited By ~ 1

Author(s):

E. Saperas ◽

H. Yang ◽

Y. Tache

Keyword(s):

Prostaglandin E2 ◽

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Paraventricular Nucleus ◽

Preoptic Area ◽

Interleukin 1 ◽

Medial Preoptic Area ◽

Anterior Hypothalamus ◽

Interleukin 1 Beta

It has been established that interleukin-1 beta (IL-1 beta) injected into the cerebrospinal fluid inhibits gastric acid secretion in rats. Brain sites of action of IL-1 beta were investigated in conscious rats implanted unilaterally with chronic hypothalamic cannula. Gastric acid secretion was monitored 2 h after pylorus ligation. Human recombinant IL-1 beta (10 ng) microinjected into the medial preoptic area, anterior hypothalamus, and paraventricular nucleus inhibited gastric acid secretion by 76-83%. IL-1 beta microinjected into the ventromedial hypothalamus and other hypothalamic sites outside of responsive sites had no effect. IL-1 beta inhibitory action in the medial preoptic area was dose related (0.1-10 ng), prevented by indomethacin (5 mg/kg ip), and mimicked by prostaglandin E2. These results show that IL-1 beta acts in the medial preoptic area/anterior hypothalamus and paraventricular nucleus to inhibit acid secretion in pylorus-ligated rats and that IL-1 beta action is likely to involve prostaglandin E2.

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Interleukin-1 Beta, Prostaglandin E2, and Immunoglobulin G Subclasses in Gingival Crevicular Fluid in Patients Undergoing Periodontal Therapy

Journal of Periodontology ◽

10.1902/jop.1996.67.8.755 ◽

1996 ◽

Vol 67 (8) ◽

pp. 755-762 ◽

Cited By ~ 33

Author(s):

David C.C. Alexander ◽

James C. Martin ◽

Philip J. King ◽

Jonathan R. Powell ◽

Janice Caves ◽

...

Keyword(s):

Prostaglandin E2 ◽

Immunoglobulin G ◽

Gingival Crevicular Fluid ◽

Interleukin 1 ◽

Periodontal Therapy ◽

Interleukin 1 Beta ◽

Immunoglobulin G Subclasses ◽

Crevicular Fluid

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Interaction between nitric oxide and prostaglandin E2 pathways in pregnant rat uteri

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1996.270.3.e471 ◽

1996 ◽

Vol 270 (3) ◽

pp. E471-E476 ◽

Cited By ~ 3

Author(s):

Y. L. Dong ◽

C. Yallampalli

Keyword(s):

Nitric Oxide ◽

Prostaglandin E2 ◽

Interleukin 1 ◽

Pge2 Production ◽

Dependent Manner ◽

Interleukin 1 Beta ◽

Uterine Contractility ◽

Pregnant Rat ◽

Nitrite Production ◽

Dose Dependent

We examined the possible interrelationship between nitric oxide (NO) and cyclooxygenase (COX) products in the uterus during pregnancy and labor. Results indicate that 1) rat uteri during labor, at term, demonstrated a 69% decrease in nitrite production and a 217% increase in prostaglandin E2 (PGE2) production compared with day 18 of pregnancy; 2) interleukin-1 beta (IL-1 beta) induced a pronounced elevation of both nitrites and PGE2 in rat uteri; 3) diethylenetriamine/NO, a donor of NO, induced a significant increase of PGE2 production by the uterus in a dose-dependent manner; 4) NG-nitro-L-arginine methyl ester, an inhibitor of NO synthesis, markedly inhibited IL-1 beta-induced nitrite and PGE2 in rat uteri; this inhibitory action was reversed by coincubation with L-arginine; 5)exogenous PGE2 significantly inhibited IL-1 beta-induced, but not constitutive, nitrite production; and 6) inhibition of endogenous PGE2 by indomethacin substantially increased IL-1 beta-induced nitrite production. Thus the interaction between NO and COX pathways might be important in the regulation of uterine contractility during pregnancy and labor.

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