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Titolo:
Low endogenous prostaglandin E-2 predisposes to relapsing inflammation in experimental rat enterocolitis
Autore:
Kandil, HM; Argenzio, RA; Sartor, RB;
Indirizzi:
N Carolina State Univ, Coll Vet Med, Dept Physiol Sci, Raleigh, NC 27606 USA N Carolina State Univ Raleigh NC USA 27606 iol Sci, Raleigh, NC 27606 USA Univ N Carolina, Dept Med, Ctr Gastrointestinal Biol & Dis, Div Digest Dis& Nutr, Chapel Hill, NC USA Univ N Carolina Chapel Hill NC USA Digest Dis& Nutr, Chapel Hill, NC USA
Titolo Testata:
DIGESTIVE DISEASES AND SCIENCES
fascicolo: 10, volume: 44, anno: 1999,
pagine: 2110 - 2118
SICI:
0163-2116(199910)44:10<2110:LEPEPT>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; FAMILIAL ADENOMATOUS POLYPOSIS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; CHRONIC INTESTINAL INFLAMMATION; IL-1 RECEPTOR ANTAGONIST; NITRIC-OXIDE SYNTHASE; BOWEL-DISEASE; FACTOR-ALPHA; EPITHELIAL-CELLS; EXPERIMENTAL COLITIS;
Keywords:
prostaglandin E-2; enterocolitis; inflammation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Argenzio, RA N Carolina State Univ, Coll Vet Med, Dept Physiol, 4700 Hillsborough St, Raleigh, NC 27606 USA N Carolina State Univ 4700 Hillsborough St Raleigh NC USA 27606
Citazione:
H.M. Kandil et al., "Low endogenous prostaglandin E-2 predisposes to relapsing inflammation in experimental rat enterocolitis", DIG DIS SCI, 44(10), 1999, pp. 2110-2118

Abstract

Intramural injection of peptidoglycan-polysaccharide (PG-PS) induces acuteenterocolitis that spontaneously relapses in Lewis but not Fischer rats. Interleukin-l (IL-1) and tumor-necrosis factor-alpha (TNF-alpha) induce prostaglandin E-2 (PGE(2)) secretion, which inhibits secretion of these cytokines by macrophages, suggesting an inhibitory feedback mechanism. We postulate that Lewis rat susceptibility to relapse is due to an imbalance between protective prostaglandins and cytokines, Female Fischer and Lewis rats were injected with PG-PS (37.5 mu g/g) or human serum albumin intramurally. Tissue IL-1 alpha and PGE(2) immunoreactivities and myeloperoxidase (MPO) activity were determined. Relapsing rats had lower PGE, and PGE(2):IL-1 alpha ratios than nonrelapsing rats (P < 0.05), In Fischer rats, 2 mg/kg/day indomethacin potentiated cecal MPO and IL-1 alpha concentrations above PG-PS alone (P < 0.05). Misoprostol treatment blocked PG-PS-induced IL-1 alpha and MPO and inhibited the potentiating effect of indomethacin on MPO and IL-1 alpha (P < 0.05). In conclusion, increased endogenous PG may be protective against relapsing inflammation in PG-PS induced enterocolitis, at least partially via inhibition of proinflammatory cytokines. An imbalance between protective prostaglandins and proinflammatory cytokines may be involved in the pathogenesis of chronic relapsing inflammation in genetically susceptible hosts.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/09/20 alle ore 17:10:01