Is the function of alveolar macrophages altered following blunt chest trauma?

The purpose of this study was to characterize the local pulmonary inflammatory environment and to elucidate alterations of alveolar macrophage (AM) functions after blunt chest trauma. Wistar rats were subjected to blunt chest trauma. AM were isolated, stimulated, and cultured. Bronchoalveolar lavage (BAL) was collected. Cytokines/chemokines were quantified in the BAL and in AM supernatants via ELISA. AM phagocytic and chemotactic activity and respiratory burst capacity were assessed. Following chest trauma, a significant increase of IL-1 beta (at 6 and 24 h) and IL-6 (at 24 h) in BAL was observed, whereas IL-10 and TNF-alpha concentrations were not altered. MIP-2 and CINC were substantially increased as early as 6 h and PGE2 early at 10 min, whereas BAL MCP-1 was not elevated until 24 h after trauma. MIP-2 release by AM isolated form trauma animals was markedly increased as early as 10 min after injury. IL-1 beta and IL-10 exhibited a late increase at 24 h. AM TNF-alpha release was increased at 6 h. At 6 or 24 h, AM from trauma animals incorporated significantly more opsonized latex beads than their sham controls, and their chemotactic activity was substantially enhanced at 24 h. AM oxidative burst capacity remained largely unchanged. Already very early after chest trauma, inflammatory mediators are present in the intraalveolar compartment. Additionally, AM are primed to release cytokines and chemokines. Blunt chest trauma also changes the phagocytic and chemotactic activity of AM. These functional changes of AM might enable them to better ward off potential pathogens in the course after trauma.