DO CIRCULATING MONOCYTES UNDERGO FUNCTIONAL CHANGES FOLLOWING BLUNT CHEST TRAUMA?

Abstract

We have previously demonstrated that alveolar macrophages (AM) are primed to release cytokines following lung contusion. So far, it has not been elucidated whether circulating monocytes (CM) undergo functional changes as well and whether posttraumatic alterations are limited to the bronchoalveolar space. We therefore sought to clarify (I) the function of CM following lung contusion and (II) the release of mediators - which predominately act on macrophages into the bronchoalveolar lavage (BAL) and blood plasma. Methods: Wistar rats were randomly allotted to 4 groups, n = 8 each. Three groups were subjected to a blast wave injury and sacrificed 10 min (TX-10 m), 6 hours (TX-6 h), and 24 hours (TX-24 h) after the trauma; another group served as control. The CM were isolated and cultured for 24 hours in the presence of 1000 ng LPS /ml. The release of TNF-α, IL-1β, MIP-2, and IL-10 was determined (ELISA) in the supernatant. In a second series, the concentrations of IL-1β, MIP-2, IL-10, and PGE2 were analyzed in the BAL and blood plasma. Results: Blunt chest trauma resulted in an excessive mediator release into the bronchoalveolar space. As soon as 10 min following trauma there was an increase (P < 0.05) of IL-10 and PGE2 in trauma animals which returned to control levels at TX-24 h. The mediator release into BAL showed a delayed kinetic with a twofold increase of IL-1β and MIP-2 (P < 0.05) in TX-24 h animals compared to controls. In sharp contrast there was no difference in the mediator concentration in the blood plasma between trauma or control animals. In agreement with these findings, there were no differences between CM of trauma and control animals with regard to the release of pro-or anti-inflammatory cytokines into the supernatant. Conclusion: The priming of AM but not CM and the excessive release of mediators which are produced by and act upon macrophages into the BAL suggests autocrine mechanism in the activation macrophages following blunt chest trauma.