The Mechanism of Steroid-Induced Fever

  1. PHYLLIS T. BODEL, M.D.;
  2. MORRIS DILLARD, M.D.; and
  3. PHILIP K. BONDY, M.D., F.A.C.P.
  1. Requests for reprints should be addressed to Philip K. Bondy, M.D., Department of Medicine, Yale University School of Medicine,
    New Haven, Conn. 06510
    .

SUMMARY

Two very dissimiliar stimuli to fever production exert their effect by the common pathway of causing activation of a process in leukocytes involving RNA and protein synthesis whereby an endogenous pyrogenic protein or polypeptide is released. The specific characteristics of steroid pyrogens in vivo, such as delayed responsiveness and unique sensitivity of human cells, are reproduced in vitro as are the chemical requirements for excitatory behavior, for the most part. In view of the fact that a common path of pyrogenic activity is followed by such disparate stimuli as gram-negative lipopolysaccharide, gram-positive cocci, tuberculin, and steroids, it seems likely that all exogenous (and some endogenous) pyrogens exert their effect by a common pathway.

Article and Author Information

  • From the Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.

  • This study was supported by grants AI 01564 and AM 00254, U. S. Public Health Service, Washington, D. C.

    • Received June 20, 1968.
    • Accepted June 23, 1968.
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