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

• Published in: Journal of clinical immunology 1989-03, Vol.9 (2), p.139-150
• Main Authors: MILLS, C. D, CALDWELL, M. D, GANN, D. S
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Burns - blood; Burns - complications; Cells, Cultured; Immune Tolerance; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunopathology; Interleukin-1 - secretion; Interleukin-2 - secretion; Killer Cells, Natural - immunology; Lymphocyte Activation; Macrophages - immunology; Male; Medical sciences; Mitogens - immunology; Plasma - immunology; Rats; Rats, Inbred F344; T-Lymphocytes - immunology; Time Factors
• ISSN: 0271-9142; 1573-2592
• DOI: 10.1007/BF00916942

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.