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Titolo:
EVIDENCE FOR AN UNKNOWN COMPONENT OF PANCREATIC ASCITES THAT INDUCES ADULT-RESPIRATORY-DISTRESS-SYNDROME THROUGH AN INTERLEUKIN-1 AND TUMORNECROSIS FACTOR-DEPENDENT MECHANISM
Autore:
DENHAM W; YANG J; NORMAN J;
Indirizzi:
UNIV S FLORIDA,DEPT SURG 112,13000 BRUCE B DOWNS BLVD TAMPA FL 33612 UNIV S FLORIDA,DEPT SURG 112 TAMPA FL 33612 UNIV S FLORIDA,PANCREAS STUDY GRP TAMPA FL 33612
Titolo Testata:
Surgery
fascicolo: 2, volume: 122, anno: 1997,
pagine: 295 - 301
SICI:
0039-6060(1997)122:2<295:EFAUCO>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
QUANTITATION; CYTOKINES; RNA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
25
Recensione:
Indirizzi per estratti:
Citazione:
W. Denham et al., "EVIDENCE FOR AN UNKNOWN COMPONENT OF PANCREATIC ASCITES THAT INDUCES ADULT-RESPIRATORY-DISTRESS-SYNDROME THROUGH AN INTERLEUKIN-1 AND TUMORNECROSIS FACTOR-DEPENDENT MECHANISM", Surgery, 122(2), 1997, pp. 295-301

Abstract

Background. The development of acute respiratory distress syndrome (ARDS) during acute pancreatitis is associated with interleukin (IL)-1 and tumor necrosis factor (TNF) gene expression within the pulmonary parenchyma. Although activated pancreatic enzymes have been thought to mediate pancreatitis-induced ARDS, they are not capable of inducing cytokine production in vitro. We hypothesized that IL-1 and TNF production in the lungs is essential to the development of ARDS and is induced by a mediator released from the inflamed pancreas. Methods. Pancreaticascites was obtained from rats after induction of bile-salt pancreatitis, cultured and assayed for IL-1, TNF, IL-6, IL-8, IL-10, interferon-gamma, and endotoxin. Sterile, cytokine-free ascites or saline (control) was subsequently administered intravenously (20 ml/kg) to healthy rats and to IL-1 R1 or TNF R1 knockout mice. Results. Animals administered intravenous ascites had a 30-fold rise in pulmonary IL-1 and TNF mRNA, as well as increased alveolar leukocytes and protein. Knockout animals devoid of active IL-1 or TNF receptors failed to develop increased alveolar protein or leukocytes. Conclusions. A component of pancreatic ascites other than activated enzymes, bacteria, or inflammatory cytokines is capable of inducing ARDS in healthy animals. The mechanismappears to be directly attributable to the activity of pulmonary IL-1and TNF.

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Documento generato il 23/09/20 alle ore 05:51:24