The numbers of leukocyte subsets in lung sections differ between intercellular adhesion molecule-1(-/-), lymphocyte function-associated antigen-1(-/-) mice and intercellular adhesion molecule-1(-/-) mice after aerosol exposure to Haemophilus influenzae type-b

In order to investigate the role of the adhesion molecules intercellular ad hesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LF A-1) in pulmonary immunological processes, leukocyte populations were stain ed immunohistochemically on cryostat lung sections of ICAM-1(-/-) and LFA-1 (-/-) mice. A further group of ICAM-1(-/-) mice was exposed to Haemophilus influenzae type-b (Hib) 24 h before being sacrificed. Comparison of the num bers of leukocytes in these groups revealed different behaviors of the leuk ocyte subsets: granulocytes were significantly increased in all three group s. Lymphocytes were increased in ICAM-1(-/-) mice, while there was no signi ficant difference in LFA-1(-/-) and even a decrease in ICAM-1(-/-) mice aft er Hib exposure. Neither in ICAM-1(-/-) nor in LFA-1(-/-) mice did macropha ges and dendritic cells (DCs) show significant differences to control anima ls. After Hib exposure, a significant elevation of DCs was observed. The fo llowing conclusions can be drawn: (1) all investigated leukocyte subsets ca n use ICAM-1- and LFA-1-independent pathways in the lungs of mice; (2) the pathways used by the leukocytes are cell-type specific: (3) ICAM-1 plays an important role in the enhanced recruitment of lymphocytes during Hib chall enge in the lung; and (4) the alternative migratory mechanisms are able to compensate for the absence of ICAM-1 or LFA-1 or even lead to increased cel l numbers. This overcompensation can be seen as a result of a balance betwe en active alternative migratory mechanisms, which takes place in the absenc e of ICAM-1 or LFA-1.