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(Journal of Leukocyte Biology. 2003;73:417-427.)
© 2003 by Society for Leukocyte Biology

Endogenous versus exogenous glucocorticoid responses to experimental bacterial sepsis

Richard Silverstein* and Donald C. Johnson{dagger}

Departments of
* Biochemistry and Molecular Biology and
{dagger} Molecular and Integrative Physiology, University of Kansas School of Medicine, Kansas City

Correspondence: Richard Silverstein, Ph.D., University of Kansas Medical Center, Department of Biochemistry and Molecular Biology, 3901 Rainbow Blvd., Kansas City, KS 66160-7421. E-mail: rsilvers{at}kumc.edu

Although lack of adrenals dramatically reduces resistance against sepsis generally, the value of glucocorticoid levels above those normally produced by stress remains controversial. An early and long-held concept is that glucocorticoid protection against lipopolysaccharides in animal models is important. Supporting this concept, C3H/HeJ mice, lacking Toll-like receptor-4 (TLR-4), and consequently, endotoxin hyporesponsive, have recently been shown to be resistant to glucocorticoid protection against live Escherichia coli. Effective antibiotic intervention, as an additional parameter and with concomitant administration of glucocorticoid, not only allows for expected antibiotic protection but also for glucocorticoid protection against E. coli or Staphylococcus aureus of mice sensitized to tumor necrosis factor {alpha}, regardless of the status of the TLR-4 receptor. TLRs, including but not limited to TLR-2, may be involved in glucocorticoid protective efficacy against Gram-positive and Gram-negative sepsis. Overlapping and possibly endotoxin-independent signaling may become important considerations.

Key Words: TNF • imipenem • Toll-like receptor • antibiotic • LPS • Gram-positive




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