Is the CD18 adhesion complex of polymorphonuclear leukocytes involved in smoke-induced lung damage? A morphometric study.

Abstract

Neutrophils are the primary vectors that produce lung parenchymal injury after smoke inhalation as a result of their transmigration through endothelial and epithelial gap junctions toward the airway surfaces. LFA-1 (CD11a/CD18) on the neutrophil surface is essential for this transmigration in many tissues. We hypothesized that anti-CD18 antibodies would block such movement and prevent lung damage. Ten sheep received nebulized cotton smoke in our standardized model of inhalation injury. The sham group (n = 2) was insufflated with air only, the second group (n = 4) was insufflated with smoke but received no antibody, and the third group (n = 4) was given monoclonal antibody R15.7 before smoke injury. A similar degree of parenchymal injury and an alveolar epithelial reparative response were measured in both groups receiving injury. Neutrophil counts in the interstitium of both injured groups were also similar. However, in the R15.7 pretreated group, neutrophils remained inside the capillary in far larger numbers (p < 0.05). The CD11/18 adhesion complex may not be necessary for the pulmonary microvascular changes associated with inhalation injury.