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   What's this?

Hamish R. Michie, FRCS; Douglas W. Wilmore, MD

Arch Surg. 1990;125(4):531-536.

Abstract
• Cytokines, products of the bodies on cells, are the major signals that orchestrate the host's response to bacterial infection. Those signals generated following infection include interleukins 1,2, and 6, interferon gamma, and tumor necrosis factor (or cachectin). Tumor necrosis factor is the only cytokine, to date, that has been shown to fulfill Koch's postulates and, thus, be causally related to host responses. Host responses to cytokines vary because of alterations in the genetic mechanism that controls cytokine production, because of an alteration in the responsiveness of the reticuloendothelial system at the time of signal induction and because of alterations in cell surface receptors. Only now are techniques evolving that can detect cytokine concentrations or production rates to relate these molecules to varying aspects of human disease. A major therapeutic goal in the future will be directed toward blocking the deleterious effects of cytokines while maintaining their protective or beneficial effects.

(Arch Surg. 1990;125:531-536)

Author Affiliations
From the Laboratories for Surgical Metabolism and Nutrition, Department of Surgery, Harvard Medical School and Brigham and Women's Hospital, Boston, Mass.

Footnotes
Accepted for publication December 6, 1989.

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

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

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

GI Complications in Patients Receiving Mechanical Ventilation
Mutlu et al.
Chest 2001;119:1222-1241.
ABSTRACT | FULL TEXT  

Effect of Mechanical Ventilation on Inflammatory Mediators in Patients With Acute Respiratory Distress Syndrome: A Randomized Controlled Trial
Ranieri et al.
JAMA 1999;282:54-61.
ABSTRACT | FULL TEXT  

Effect of Prednisolone on the Systemic Response and Wound Healing After Colonic Surgery
Schulze et al.
Arch Surg 1997;132:129-135.
ABSTRACT  

Different endotoxin release and IL-6 plasma levels after antibiotic administration in surgical intensive care patients
Holzheimer et al.
Innate Immunity 1996;3:261-267.
ABSTRACT  

Polymyxin B Prevents Increased Sympathetic Activity and Alveolar Macrophage Tumor Necrosis Factor Release in Parenterally Fed Rats
Johnson et al.
Arch Surg 1995;130:1294-1300.
ABSTRACT  

TPN-Induced Sympathetic Activation Is Related to Diet, Bacterial Translocation, and an Intravenous Line
Helton et al.
Arch Surg 1995;130:209-214.
ABSTRACT  

The Horror Autotoxicus and Multiple-Organ Failure
Baue
Arch Surg 1992;127:1451-1462.
ABSTRACT  

The Hypothalamic-Pituitary-Adrenal--Immune Axis: A Critical Assessment
Lilly and Gann
Arch Surg 1992;127:1463-1474.
ABSTRACT  

Effect of Combined Prednisolone, Epidural Analgesia, and Indomethacin on the Systemic Response After Colonic Surgery
Schulze et al.
Arch Surg 1992;127:325-331.
ABSTRACT  

Organ Interactions in Sepsis: Host Defense and the Hepatic-Pulmonary Macrophage Axis
Callery et al.
Arch Surg 1991;126:28-32.
ABSTRACT  

Tumor Necrosis Factor and Endotoxin Can Cause Neutrophil Activation Through Separate Pathways
Moore et al.
Arch Surg 1991;126:70-73.
ABSTRACT