Role of β1 β2 integrins and ICAM-1 in lung injury after deposition of IgG and IgA immune complexes

摘要: After intrapulmonary deposition of IgG or IgA immune complexes, injury has been recently shown to be CD18-dependent in both cases and E-selection-dependent only the former case. In our studies further evaluation requirements for beta 1 2 integrins intercellular adhesion molecule-1 (ICAM-1) undertaken. complex model, which is neutrophil dependent, anti-CD11a reduced (as measured by changes permeability hemorrhage) 61 43%, respectively, whereas a newly developed anti-CD11b produced minimal protection (16 19%, respectively). Treatment rats with increasing doses (1.5- 3.0-fold) antibody rat CD11b failed demonstrate additional protective effects this model injury. Anti-ICAM-1 parameters 78%, while anti-VLA-4 40 35%, respectively. There were reductions lung content myeloperoxidase, roughly corresponding interventions. injury, macrophages appear effector cells, (permeability 36 33%, 63 67%, anti-ICAM-1 56%, 77 62%, The cell bronchoalveolar lavage fluids revealed that have reflect interventions models complex-induced These findings suggest that, VLA-4 ICAM-1 are required, although lymphocyte function-associated Ag-1 predominant integrin requirement Mac-1 Thus, engagement molecules manner leading depends on nature inflammatory stimulus type phagocytic cells involved development