The requirement of intercellular adhesion molecule-1 for neutrophil respiratory burst in the pulmonary circulation of rats infused with endotoxin.

Abstract

Recently, we demonstrated direct evidence of respiratory burst of the neutrophil in the pulmonary circulation of the endotoxin-infused rat (Am. J. Respir. Crit. Care Med. 1995;152:348-354). To determine the role of intercellular adhesion molecule-1 (ICAM-1) in this model, we neutralized ICAM-1 using antirat ICAM-1 monoclonal antibody (mAb) 1A29. We observed and measured the number of sticking leukocytes and the amount of hydrogen peroxide (H2O2) in the pulmonary circulation of the endotoxin-infused rat by means of a fluoro-imaging technique. The rats received 4.5 mg/kg/h of endotoxin for 2 h. Ten rats received 2 mg/kg of mAb 1A29 20 min before the intravenous infusion of endotoxin. Although the pretreatment with mAb 1A29 did not reduce the number of leukocytes sticking to the pulmonary capillaries, it almost completely inhibited the H2O2 production of leukocytes in the rat lung infused with endotoxin. We confirmed that the leukocytes that produced H2O2 were neutrophil by an electron microscopic cerium technique. We conclude that, although ICAM-1 is not necessary for neutrophil to stick to the capillary in the rat pulmonary circulation infused with endotoxin, ICAM-1 is required for neutrophil H2O2 production in this model.