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. 132 No. 12, December 1997 TABLE OF CONTENTS
  Archives
  •  Online Features
  PAPERS
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •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?

Suppression of Natural Killer Cell Activity in Patients With Fracture/Soft Tissue Injury

Carl J. Hauser, MD; Pratibha Joshi, PhD; Quintus Jones; Xinchun Zhou, MD, PhD; David H. Livingston, MD; Robert F. Lavery, MA

Arch Surg. 1997;132(12):1326-1330.


Abstract

Background
Natural killer cells (NKCs) participate in "innate" cell-mediated immunity. Fracture/soft tissue injuries are cytokine rich and may influence cell-mediated immunity.

Objective
To study the effects of fracture cytokines on NKC function.

Design
A case-control study.

Setting
A level I trauma center and laboratory in a university medical center.

Participants
Patients requiring open fracture fixation and healthy volunteers.

Interventions
Fracture supernatants and peripheral plasma were collected during open fracture fixation. Volunteer mononuclear cells were used as effector (NKC) sources. Mononuclear cells were preincubated with fracture supernatants, paired peripheral plasma, or normal plasma under various conditions.

Main Outcome Measures
Natural killer cell lysis of K562 target cells was assessed by chromium 51 release.

Results
Fracture supernatants suppressed NKC function more rapidly than peripheral plasma. Fracture supernatants from 1 to 4 days after injury were most suppressive. Inactivation of complement and reactive oxygen species failed to restore lysis. Neutralizing antibodies to interleukin 4 and interleukin 10 further suppressed lysis. Antibodies to transforming growth factor β1 failed to restore lysis. The addition of interferon {gamma} did not restore lysis but the addition of interleukin 12 did.

Conclusions
Fracture supernatants and peripheral plasma from patients with fractures suppress NKCs. The responsible mediators may be concentrated in fracture/ soft tissue injuries. Responses to manipulation of the cytokine environment suggest that fracture cytokines may impair cooperation between NKCs and accessory cells.

Arch Surg. 1997;132:1326-1330



Author Affiliations

From the Departments of Surgery, UMDNJ—New Jersey Medical School, Newark (Drs Hauser and Livingston and Mr Lavery); and the University of Mississippi Medical Center, Jackson (Drs Joshi and Zhou and Mr Jones).



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?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Immunologic Responses to Critical Injury and Sepsis
Smith et al.
J Intensive Care Med 2006;21:160-172.
ABSTRACT  

Prostaglandin E2 Suppressed IL-15-Mediated Human NK Cell Function Through Down-Regulation of Common {{gamma}}-Chain
Joshi et al.
J. Immunol. 2001;166:885-891.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1997 American Medical Association. All Rights Reserved.