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. 131 No. 12, December 1996 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?

Dominance of T-Helper 2–Type Cytokines After Severe Injury

Vivian E. Mack; Martin D. McCarter, MD; Hassan A. Naama, MD; Steve E. Calvano, PhD; John M. Daly, MD

Arch Surg. 1996;131(12):1303-1309.


Abstract

Objective
To determine whether severe injury leads to a dominance of splenocyte-produced T-helper (Th) 2–type cytokines, partly explaining the observed defects in cellular immune responses in the posttraumatic state.

Design
Female BALB/c mice (n=6 per group) were randomized to receive anesthesia alone (control) or a combined femur fracture and a hemorrhage of 40% of total blood volume (trauma). On days 1 and 7 after injury, mice were killed and spleens were harvested. Splenocytes were stimulated in vitro with 2.5 µg of concanavalin A per milliliter. After 72 hours of incubation, splenocyte proliferation was determined by means of tritiated thymidine uptake. Production of interferon-{gamma} and interleukins (IL) -2, -4, -5, -6, and -10 from supernatants harvested after 24 or 72 hours of incubation was quantified by enzyme-linked immunosorbent assay.

Setting
Surgical immunology research laboratory of a medical college.

Main Outcome Measures
Mouse spleen weight, splenocyte number, and proliferation in addition to cytokine production (interferon-{gamma}, IL-2, IL-4, IL-5, IL-6, and IL-10).

Results
Splenocyte proliferative capacity was unaffected at day 1 after injury but was significantly suppressed (P<.05) by day 7 after injury. Similarly, there were no changes in splenocyte cytokine production in a comparison of control and injured mice at day 1. At day 7, however, there was nearly a 90% decrease in the Th1-type cytokines (interferon-{gamma} and IL-2; P≤.002) and at least a 30% increase in the Th2-type cytokines IL-4, IL-5, IL-6, and IL-10 (P=.06 for IL-6 and P≤.03 for IL-4, IL-5, and IL-10).

Conclusions
These data indicate that a shift to a Th2-type splenocyte cytokine response occurs late, at 7 days after injury. Modulation of Th cell cytokine responses may partially explain defects observed in cellular immune responses in postinjury states. Therapies that augment Th1-type cytokine production and/or neutralize Th2-type cytokines may prove beneficial.

Arch Surg. 1996;131:1303-1309



Author Affiliations

From the Department of Surgery, The New York Hospital—Cornell University Medical Center, New York, NY.



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

Murine dendritic cell antigen-presenting cell function is not altered by burn injury
Fujimi et al.
J. Leukoc. Biol. 2009;85:862-870.
ABSTRACT | FULL TEXT  

Severe tissue trauma triggers the autoimmune state systemic lupus erythematosus in the MRL/++ lupus-prone mouse
Anam et al.
Lupus 2009;18:318-331.
ABSTRACT  

Invited review: Deterioration of the immune system after trauma: signals and cellular mechanisms
Flohe et al.
Innate Immunity 2008;14:333-344.
ABSTRACT  

Comparison of longitudinal leukocyte gene expression after burn injury or trauma-hemorrhage in mice
Lederer et al.
Physiol. Genomics 2008;32:299-310.
ABSTRACT | FULL TEXT  

Injury Enhances Resistance to Escherichia coli Infection by Boosting Innate Immune System Function
Maung et al.
J. Immunol. 2008;180:2450-2458.
ABSTRACT | FULL TEXT  

Burn-induced immunosuppression: attenuated T cell signaling independent of IFN-{gamma}- and nitric oxide-mediated pathways
Duan et al.
J. Leukoc. Biol. 2008;83:305-313.
ABSTRACT | FULL TEXT  

Intervention at the Level of the Neuroendocrine-Immune Axis and Postoperative Pneumonia Rate in Long-term Alcoholics
Spies et al.
Am. J. Respir. Crit. Care Med. 2006;174:408-414.
ABSTRACT | FULL TEXT  

General Anesthesia Delays the Inflammatory Response and Increases Survival for Mice with Endotoxic Shock
Fuentes et al.
CVI 2006;13:281-288.
ABSTRACT | FULL TEXT  

Enhanced Regulatory T Cell Activity Is an Element of the Host Response to Injury
Choileain et al.
J. Immunol. 2006;176:225-236.
ABSTRACT | FULL TEXT  

CD4+CD25+ Regulatory T Cells Control Innate Immune Reactivity after Injury
Murphy et al.
J. Immunol. 2005;174:2957-2963.
ABSTRACT | FULL TEXT  

Burn Injury Initiates a Shift in Superantigen-Induced T Cell Responses and Host Survival
Zang et al.
J. Immunol. 2004;172:4883-4892.
ABSTRACT | FULL TEXT  

Injury, sepsis, and the regulation of Toll-like receptor responses
Murphy et al.
J. Leukoc. Biol. 2004;75:400-407.
ABSTRACT | FULL TEXT  

Interferon-{gamma} increases monocyte HLA-DR expression without effects on glucose and fat metabolism in postoperative patients
de Metz et al.
J. Appl. Physiol. 2004;96:597-603.
ABSTRACT | FULL TEXT  

Stroke-induced Immunodeficiency Promotes Spontaneous Bacterial Infections and Is Mediated by Sympathetic Activation Reversal by Poststroke T Helper Cell Type 1-like Immunostimulation
Prass et al.
JEM 2003;198:725-736.
ABSTRACT | FULL TEXT  

Hypertonicity rescues T cells from suppression by trauma-induced anti-inflammatory mediators
Loomis et al.
Am. J. Physiol. Cell Physiol. 2001;281:C840-C848.
ABSTRACT | FULL TEXT  

Immunology of trauma
Cook
Trauma 2001;3:79-88.
ABSTRACT  

Protective Effects of Early Interleukin 10 Antagonism on Injury-Induced Immune Dysfunction
Lyons et al.
Arch Surg 1999;134:1317-1324.
ABSTRACT | FULL TEXT  

Male Gender Is a Risk Factor for Major Infections After Surgery
Offner et al.
Arch Surg 1999;134:935-940.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1996 American Medical Association. All Rights Reserved.