Abstract
ABOUT five out of 1,000 patients admitted to hospital develop bacterial sepsis leading to shock1, the mortality rate for which is high despite antibiotic therapy2. The infection results in hypotension and poor tissue perfusion, and eventually leads to the failure of several organ systems. Bacterial endotoxin is thought to be the direct cause of shock in Gram-negative sepsis, because it can cause shock in animals3, and antibodies against endotoxin prevent Gram-negative shock in animals4 and in humans5–7. But, the symptoms of septic shock are the result of the actions of host cytokines induced by the endotoxin. The cytokiue interleukin-1 has been implicated as an important mediator of septic shock because it can induce tachycardia and hypotension and act synergistically with tumour necrosis factor to cause tissue damage8 and death9. We now report that a specific interleukin-1 receptor antagonist reduces the lethality of endotoxin-induced shock in rabbits, indicating that interleukin-1 does indeed play an important part in endotoxin shock.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Rent or buy this article
Prices vary by article type
from$1.95
to$39.95
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
References
Lode, H. Arzneimitteltherapie 1, 82–89 (1983).
Kreger, B. E., Crave, D. E. & McCabe, W. R.,Am. J. Med. 68, 343–355 (1980).
Guenter, C. A., Florcica, V. & Hinshaw, B. J. J. appl. Physiol. 26, 780–786 (1969).
Ziegler, E. J., Douglas, H., Sherman, J. E., Davis, C. E. & Braude, A. I. J. Immun. 111, 433–438 (1973).
Ziegler, E. J. et al. New Engl. J. Med. 307, 1255–1230 (1982).
Ziegler, E., Sprung, C., Straube, R. & Sadoff, J. Clin. Res. 38, 304A (1990).
Gorelick, K. J., Schein, R. M. H., Maclntyre, N. R., Emmanuel, G. & Bernard, G. R. Crit. Care Med. 18, S253 (1990).
Okusawa, S., Gelfand, J. A., Ikejima, T., Connolly, R. J. & Dinarello, C. A. J. clin. Invest. 81, 1162–1172 (1988).
Everaerdt, B., Brouckaert, P., Shaw, A. & Fiers, W. Biochem. biophys. Res. Commun., 163, 378–385 (1989).
Hannum, C. H. et al. Nature 343, 336–340 (1990).
Eisenberg, S. P. et al. Nature 343, 341–346 (1990).
Arend, W. P., Welgus, H. G., Thompson, R. C. & Eisenberg, S. P. J. clin. Invest. 85, 1694–1697 (1990).
Mancini, G., Carbonnara, A. O. & Heremans, J. Immunochemistry 2, 235–254 (1965).
Michie, H. R. et al. New Engl. J. Med. 318, 1481–1486 (1988).
Tracey, K. J. et al. Science 234, 470–474 (1986).
Tracey, K. J. et al. Nature 330, 662–664 (1987).
Beutler, B., Milsark, I. & Cerami, A. Science 229, 869–871 (1985).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Ohlsson, K., Björk, P., Bergenfeldt, M. et al. Interleukin-1 receptor antagonist reduces mortality from endotoxin shock. Nature 348, 550–552 (1990). https://doi.org/10.1038/348550a0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/348550a0
This article is cited by
-
Inflammasome-mediated GSDMD activation facilitates escape of Candida albicans from macrophages
Nature Communications (2021)
-
Mediatory roles of leukotriene B4 receptors in LPS-induced endotoxic shock
Scientific Reports (2019)
-
Protective Effects of Nobiletin Against Endotoxic Shock in Mice Through Inhibiting TNF-α, IL-6, and HMGB1 and Regulating NF-κB Pathway
Inflammation (2016)
-
Choc septique : mécanismes du décès
Réanimation (2015)
-
Enhanced monocyte chemoattractant protein-1 production in aging mice exaggerates cardiac depression during endotoxemia
Critical Care (2014)
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.