Evidence of a plasma-mediated "window" of immunodeficiency in rats following trauma.

The etiology of immunodeficiency following trauma was investigated. Plasma collected from Fischer rats 1-8 hr following a 40% surface area thermal injury (TI) displays immunosuppressive activity (ISA). Peak ISA (4 hr) exceeded 90% inhibition of Con A3-induced proliferation of normal spleen cells. Splenic macrophage IL-1 secretion and NK activity are also inhibited by 4-hr TI plasma. Most importantly, these same cellular immune functions decline in rats by 4 hr following TI. After a further decline by 16 hr (IL-1 = 19.8% and NK activity = 40% of normal), these cellular immune functions rebound toward normal values by 2 days following TI. Thus, ISA in plasma is both temporally and functionally linked to the cellular immune defects observed. Sham-treatment rats display a similar, although less marked, pattern of plasma-linked transient cellular immune defects indicating a role for stress in these responses. ISA is abolished by mild heat (56 degrees C for 30 min) and wholly contained in the greater than 10-kD fraction of plasma. Together, these results provide evidence that previously unrecognized molecules in plasma induce a "window" of immunodeficiency early following trauma.