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Transmigration of neutrophils (PMNs) from the vasculature into inflamed tissues, mediated by interactions between PMNs and adhesion molecules on endothelial cells, is an essential aspect of inflammation. The crucial adhesion molecules include junctional adhesion molecule (JAM)-A. Investigation of the role of this molecule in models of inflammatory disease has been limited, however, and results in different disease models have varied. No previous study has addressed JAM-A in lung disease or effects on oxidant stress and proinflammatory cytokines. We use JAM-A knockout mice and blocking antibodies to investigate the role of JAM-A in a murine model of acute lung injury (ALI). With either experimental system, we find that absence of JAM-A activity significantly reduces migration of PMNs into the alveolar space, with a resulting decrease in oxidative stress. However, there is no reduction in whole lung activity of PMN-associated myeloperoxidase, presumably reflecting the histologically observed retention of PMNs in lung tissue. Activity of these retained PMNs may account for our failure to find significant change in markers of lung oxidative stress or cytokine and chemokine levels in plasma, lung, and bronchoalveolar lavage fluid. We likewise see no JAM-A-related changes in markers of capillary permeability or lung injury. A similar lack of congruence between effects on PMN migration and tissue injury has been reported in other disease models and for other adhesion molecules in models of ALI. Our results thus confirm the crucial role of JAM-A in PMN transmigration but demonstrate that transmigration is not essential for other aspects of inflammation or for lung injury in ALI.

Effects of JAM-A deficiency or blocking antibodies on neutrophil migration and lung injury in a murine model of ALI