Role of integrins and intracellular adhesion molecule-1 in lung injury after intestinal ischemia-reperfusion

Kuzu M., Koksoy C., Kuzu I., Gurhan I., Ergun H., Demirpence E.

AMERICAN JOURNAL OF SURGERY, sa.1, ss.70-74, 2002 (SCI-Expanded) identifier identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2002
  • Doi Numarası: 10.1016/s0002-9610(01)00846-7
  • Dergi Adı: AMERICAN JOURNAL OF SURGERY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.70-74
  • Anahtar Kelimeler: ischemia/reperfusion, lung, intestines, leukocytes, adhesion molecules, integrins, LEUKOCYTE ADHESION, INFLAMMATORY INJURY, MONOCLONAL-ANTIBODY, BETA-2 INTEGRINS, NEUTROPHILS, TRAUMA, CD18, GLYCOPROTEIN, REDUCTION, ADHERENCE
  • Ankara Üniversitesi Adresli: Evet

Özet

Background: We tested the hypothesis that lung injury after intestinal ischemia-reperfusion (IR) requires the activation of CD11/CD18 glycoprotein complex and its ligand, intracellular adhesion molecule-1 (ICAM-1), on pulmonary endothelial surface. Methods: Rats were assigned to one of six groups including sham operation, intestinal IR (60/120 min) and IR plus treatment with one of the following antibodies against CD11a, CD11b, CD18, and ICAM-1. Pulmonary microvascular permeability, neutrophil accumulation, and expression of adhesion molecules were evaluated. Results: Intestinal IR resulted in lung injury characterized by a marked increase in microvascular permeability, neutrophil accumulation and upregulated expression of leukocyte integrins and ICAM-1. The increase in pulmonary microvascular permability and neutrophil accumulation elicited by intestinal reperfusion was effectively prevented by administration of blocking antibodies against ICAM-1, CD11, and CD18. Conclusions: These results indicate that adhesion molecules contribute to the lung injury after intestinal IR. Immunoneutralization of certain of these adhesion molecules may present intestinal IR-induced lung injury. (C) 2002 Excerpta Medica, Inc. All rights reserved.