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Titolo:
Laparotomy prevents lethal endotoxemia in a murine sequential insult modelby an IL-10-dependent mechanism
Autore:
Back, MR; Sarac, TP; Moldawer, LL; Welborn, MB; Seeger, JM; Huber, TS;
Indirizzi:
Univ Florida, Coll Med, Dept Surg, Gainesville, FL 32610 USA Univ FloridaGainesville FL USA 32610 ept Surg, Gainesville, FL 32610 USA
Titolo Testata:
SHOCK
fascicolo: 2, volume: 14, anno: 2000,
pagine: 157 - 162
SICI:
1073-2322(200008)14:2<157:LPLEIA>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; MULTIPLE ORGAN DYSFUNCTION; AORTIC-ANEURYSM REPAIR; INTERLEUKIN-10 IL-10; HEPATIC ISCHEMIA/REPERFUSION; SURGICAL-TREATMENT; VISCERAL ISCHEMIA; DOWN-REGULATION; LIPOPOLYSACCHARIDE;
Keywords:
multiple organ dysfunction; multiple organ failure; cytokines; visceral ischemia and reperfusion; two-hit model; tolerance; endotoxemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Huber, TS Univ Florida, Coll Med, Dept Surg, POB 100286, Gainesville, FL 32610 USA Univ Florida POB 100286 Gainesville FL USA 32610 e, FL 32610 USA
Citazione:
M.R. Back et al., "Laparotomy prevents lethal endotoxemia in a murine sequential insult modelby an IL-10-dependent mechanism", SHOCK, 14(2), 2000, pp. 157-162

Abstract

Multiple organ dysfunction and death are common sequelae after mesenteric ischemia-reperfusion injury as seen with mesenteric revascularization and thoracoabdominal aortic aneurysm repair. A second insult such as bacterial pneumonia occurring subsequent to the ischemia-reperfusion injury may contribute to these untoward effects. We hypothesized the sequential visceral/lower torso ischemia-reperfusion and endotoxemia in a murine model would increase the magnitude of the proinflammatory cytokine response and decrease survival. C57BL/6 mice underwent 20 min of supraceliac occlusion (IR), sham laparotomy (LAP), or no initial insult (CTRL) followed by intraperitoneal injection of a lethal dose of endotoxin (LPS [lipopolysaccharide 50 mg/kg] or saline vehicle at 24 h. Serum cytokine levels were measured by enzyme-linked immunosorbent assay (IL-10, IL-6) or WEHI bioassay [tumor necrosis factor(TNF)], and survival was determined at 5 days. The role of IL-10 on the TNF response and survival was examined in a subset of mice given mouse anti IL-10 IgM (25 mg/kg intraperitoneally) 2 h prior to the initial insult. Survival after LPS was significantly different (P < 0.05) among the treatment groups (IR, 64%; LAP, 55%; CTRL, 11%) and appeared to trend directly with the magnitude of the initial operation. The serum IL-10 levels in the IR and LAP groups were significantly increased 4 h after the initial insult and remained elevated at 24 h. Peak serum TNF levels after LPS were significantlylower in the IR and LAP groups. Administration of anti IL-10 IgM resulted in uniform mortality and a significant increase in the peak TNF levels after LPS administration for all initial treatment groups. Endogenous production of IL-10 following [aparotomy downregulates the TNF response and improvessurvival after endotoxemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 09:15:57