Human monocyte plasminogen activator production: correlation to altered Mphi-T lymphocyte interaction.

Previous work established that about 40 to 50% of asplenic trauma patients develop peripheral blood populations that are mitogen-hyporesponsive. This mitogen hyporesponsiveness is partially mediated by aberrant monocyte (Mϕ) function. Mononuclear phagocytes (Mϕ) play an essential role in mitogen-induced lymphocyte proliferation. In this study, asplenic patients were assessed for a correlation between alterations in lymphocyte independent Mϕ functions and development of mitogen hyporesponsiveness due to decreased Mϕ-T cell interactions. Mϕ from 14 asplenic trauma patients were assessed for their plasminogen activator (PA), tissue procoagulant factor (TF), and lysozyme activity. The response of the mononuclear cell population of these patients to phytohemagglutinin (PHA) was simultaneously assayed. Fifty percent (7/14) of these patients produced Mϕ that showed significantly depressed PA production, augmented TF generation, and unaltered lysozyme activity. Depressed Mϕ PA function was positively correlated to the development of PHA hyporesponsiveness; augmented Mϕ TF activity was negatively correlated to both altered Mϕ PA production and PHA hyporesponsiveness. Maximal alterations in PA Mϕ and TF function occurred at 8 to 13 days post-injury, and onset of these Mϕ aberrations appeared to precede the appearance of the PHA hyporesponsiveness and depressed Mϕ-T cell interaction. These data suggest monitoring of alterations in Mϕ PA and TF functions may allow detection of traumainduced aberrations in Mϕ-T cell interaction and consequent depressed immune function.