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. Sp...

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Bibliographic Details
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
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Summary: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.
ISSN:0271-9142
1573-2592
DOI:10.1007/BF00916942