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.
Mills
C D
CD
Department of Surgery, Rhode Island Hospital, Brown University School of Medicine, Providence 02902.
Caldwell
M D
MD
Gann
D S
DS
D000818:Animals; D002056:Burns / Q000097:blood / Q000150:complications*; D002478:Cells, Cultured; D007108:Immune Tolerance; D007375:Interleukin-1 / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology; D008213:Lymphocyte Activation; D008264:Macrophages / Q000276:immunology; D008297:Male; D008934:Mitogens / Q000276:immunology; D010949:Plasma / Q000276:immunology*; D051381:Rats; D011916:Rats, Inbred F344; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors
D007375:Interleukin-1; D007376:Interleukin-2; D008934:Mitogens