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

Abstract.

In order to investigate the role of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) in pulmonary immunological processes, leukocyte populations were stained 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 numbers of leukocytes in these groups revealed different behaviors of the leukocyte subsets: granulocytes were significantly increased in all three groups. Lymphocytes were increased in ICAM-1^–/– mice, while there was no significant difference in LFA-1^–/– and even a decrease in ICAM-1^–/– mice after Hib exposure. Neither in ICAM-1^–/– nor in LFA-1^–/– mice did macrophages and dendritic cells (DCs) show significant differences to control animals. After Hib exposure, a significant elevation of DCs was observed. The following conclusions can be drawn: (1) all investigated leukocyte subsets can 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 challenge 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 cell numbers. This overcompensation can be seen as a result of a balance between active alternative migratory mechanisms, which takes place in the absence of ICAM-1 or LFA-1.