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Titolo:
Effects of inhibition of PAF, ICAM-1 and PECAM-1 on gut barrier failure caused by intestinal ischemia and reperfusion
Autore:
Sun, Z; Wang, X; Lasson, A; Bojesson, A; Annborn, M; Andersson, R;
Indirizzi:
Dept Surg, Lund, Sweden Dept Surg Lund SwedenDept Surg, Lund, Sweden Univ Lund, Malmo Univ Hosp, Lund, Sweden Univ Lund Lund SwedenUniv Lund, Malmo Univ Hosp, Lund, Sweden
Titolo Testata:
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
fascicolo: 1, volume: 36, anno: 2001,
pagine: 55 - 65
SICI:
0036-5521(200101)36:1<55:EOIOPI>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERCELLULAR-ADHESION MOLECULE-1; ACUTE-PANCREATITIS; ENDOTHELIAL-CELLS; NEUTROPHIL; EXPRESSION; MECHANISM; INJURY; INVOLVEMENT; DISEASE; RAT;
Keywords:
adhesion molecules; barrier; cytokine; endothelium; epithelium; leukocyte; permeability; protease inhibitors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Andersson, R Univ Lund Hosp, Dept Surg, S-22185 Lund, Sweden Univ Lund Hosp Lund Sweden S-22185 rg, S-22185 Lund, Sweden
Citazione:
Z. Sun et al., "Effects of inhibition of PAF, ICAM-1 and PECAM-1 on gut barrier failure caused by intestinal ischemia and reperfusion", SC J GASTR, 36(1), 2001, pp. 55-65

Abstract

Background: The role of cell adhesion molecules and transmigration of PMNsthrough the endothelial barrier is probably essential in intestinal ischemia and reperfusion (I/R)-induced gut barrier dysfunction. Although cytokines are released in I/R, it is unclear whether cytokines directly increase permeability or if this phenomenon requires both expression of cell adhesion molecules and PMN adhesion-activation. Endothelial barrier dysfunction plays an important role in the pathogenesis of multiple organ dysfunction syndrome, inducing gut barrier failure, but the mechanisms are not fully understood. The purpose of this study was to evaluate the potential therapeutic value of inhibition of platelet activating factor (PAF), intercellular adhesion molecule-1 (ICAM-1), and platelet endothelial cell adhesion molecule-1 (PECAM-1) in gut barrier dysfunction induced by intestinal I/R. Methods: A PAF antagonist (lexipafant, BB-882) and monoclonal antibodies against rat ICAM-1 (anti-ICAM-1-MAb) and PECAM-1 (anti-PECAM-1-MAb) were used in a model of gut barrier dysfunction caused by intestinal ischemia for 40 min and concomitant reperfusion for 12 h in the rat, and endothelial permeability, myeloperoxidase activity, interleukin-1 beta, and protease inhibitor levels were evaluated. Results: The endothelial permeability and tissue leukocyte recruitment in the distal small intestine significantly increased in rats with I/R treated with saline. Proteolytic activity in plasma was evident by low levels of the three measured plasma protease inhibitors. These changes were, to different degrees, reduced by treatment with lexipafant, anti-ICAM-1-MAb, or anti-PECAM-1-MAb. Alterations in systemic levels of interleukin-1 beta paralleled the changes found in gut barrier permeability and leukocytetrapping. Conclusions: Our results suggest that treatment with the PAF inhibitor lexipafant and monoclonal antibodies against ICAM-1 or, seemingly most efficient, PECAM-1 reduces the severity of IIR-associated intestinal dysfunction, associated with a decrease in systemic concentrations of IL-1 beta local leukocyte recruitment, and partly restoring plasma protease inhibitor levels.

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Documento generato il 08/04/20 alle ore 10:12:17