L-selectin and intercellular adhesion molecule 1 mediate lymphocyte migration to the inflamed airway/lung during an allergic inflammatory response inan animal model of asthma

T lymphocytes play a critical role in the development of allergic inflammat ion in asthma, Early in the allergic response, T lymphocytes migrate from t he circulation into the lung to initiate and propagate airway inflammation, The adhesion molecules that mediate lymphocyte entry into inflamed lung ha ve not been defined, This study directly examined the roles of L-selectin a nd intercellular adhesion molecule 1 (ICAM-1) in lymphocyte migration to th e lung during an allergic inflammatory response in an animal model of asthm a, Short-term (1 hour) in vivo migration assays and various combinations of adhesion molecule-deficient and wild-type mice were used. Migration of in vivo activated lymphocytes into inflamed lung was significantly greater tha n entry of resting lymphocytes into noninflamed lung (24.5% +/- 2.7% vs 9.5 % +/- 1.3%, P = .001). Migration of activated lymphocytes into inflamed lun g was inhibited by 30% in the absence of L-selectin (17.3% +/- 1.3%, P = .0 4), 47% in the absence of cell surface ICAM-1 (13.0% +/- 2.5%, P = .01), an d 47% in the absence of endothelial ICAM-1 (13.0% +/- 2.5%, P = .01), Loss of ICAM-1 on both lymphocytes and lung endothelium inhibited lymphocyte mig ration by 60% (9.8% +/- 1.8%, P = .002), These endings demonstrate dear rol es for both L-selectin and ICAM-1 in lymphocyte migration to the lung durin g an allergic inflammatory response, with ICAM-1 playing a greater role.