You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 128 No. 2, February 1993 TABLE OF CONTENTS
  Archives
  •  Online Features
  PAPERS PRESENTED AT THE 12TH ANNUAL MEETING OF THE SURGICAL INFECTION SOCIETY, LOS ANGELES, CALIF, APRIL 9, 1992
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Elaboration of Interleukin 1–Receptor Antagonist Is Not Attenuated by Glucocorticoids After Endotoxemia

Alfred A. Santos, MD; Marcus R. Scheltinga, MD; Elizabeth Lynch, MA; Elaine F. Brown, MA; Pornsi Lawton, MA; Elizabeth Chambers, MA; Jeffrey Browning, PhD; Charles A. Dinarello, MD; Sheldon M. Wolff, MD; Douglas W. Wilmore, MD

Arch Surg. 1993;128(2):138-144.


Abstract

• The body's response to infection/inflammation is initiated by the elaboration of cytokines, such as tumor necrosis factor, interleukin 1-β (IL-1-β), IL-6, and IL-8. Cytokines, in turn, stimulate the pituitary-adrenal axis, and it has been suggested that the corticosteroids elaborated serve as negative feedback signals to diminish inflammatory events. To test this hypothesis, we administered hydrocortisone shortly before endotoxin administration to normal volunteers. Steroids greatly reduced the clinical response to endotoxin and attenuated the appearance of tumor necrosis factor, IL-6, and IL-8 in the circulation. In contrast, IL-1–receptor antagonist, a competitive antagonist of the IL-1 receptor, was unaffected by steroid administration. These data suggest that IL-1–receptor antagonist may act in synergism with corticosteroids to reduce inflammation. Elevation of concentrations of these two factors, corticosteroids and IL-1–receptor antagonist, in plasma appears to be the mechanism used by the body to overcome the effects of inflammatory cytokines.

(Arch Surg. 1993;128:138-144)



Author Affiliations

From the Laboratory for Surgical Metabolism and Nutrition, Department of Surgery, Brigham and Women's Hospital, Boston, Mass, and Harvard Medical School, Boston (Drs Santos, Scheltinga, and Wilmore, and Mss Brown and Chambers); Department of Medicine, Division of Geographic Medicine and Infectious Diseases, Tufts University Medical School, New England Medical Center Hospital, Boston (Ms Lynch and Drs Dinarello and Wolff); and Department of Cell Biology, Biogen Inc, Cambridge, Mass (Ms Lawton and Dr Browning).


Footnotes

Accepted for publication November 7, 1992.

Presented at the 12th Annual Meeting of the Surgical Infection Society, Los Angeles, Calif, April 9, 1992.

Reprint requests to Laboratory for Surgical Metabolism and Nutrition, Department of Surgery, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115 (Dr Wilmore).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1993 American Medical Association. All Rights Reserved.