 |
 |

Identification of a Novel Tumor Necrosis Factor Cachectin From the Livers of Burned and Infected Rats
Christopher Keogh;
Yuman Fong, MD;
Michael A. Marano, MD;
Sophie Seniuk;
Wei He, MD;
Annabel Barber, MD;
Joseph P. Minei, MD;
Diane Felsen, PhD;
Stephen F. Lowry, MD;
Lyle L. Moldawer, PhD
Arch Surg. 1990;125(1):79-85.
Abstract
 |  |
Tumor necrosis factor (TNF- )/cachectin is a monocyte/macrophage-derived cytokine implicated as a proximal mediator of many of the catastrophic host responses to infection or endotoxin. However, circulating levels of TNF- /cachectin have only been episodically detected in hospitalized patients with life-threatening bacterial infections. In the present report, increased quantities of immune-reactive TNF- /cachectin were recovered from the livers of rats 3 days following a lethal burn and infection. Two species of TNF- /cachectin were detected, one of approximately 29 kd and the other 17 kd, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In murine peritoneal macrophages and rat Kupffer cells stimulated in vitro with endotoxin, a 29-kd cell-associated and 17-kd secreted form were also detected. We conclude that the increased appearance in vivo of a 29-kd form of TNF- /cachectin from the livers of lethally burned and infected rats represents a novel cell-associated form of the protein.
(Arch Surg. 1990;125:79-85)
Author Affiliations
From the Laboratory of Surgical Metabolism (Mr Keogh and Drs Fong, Marano, He, Barber, Minei, Lowry, and Moldawer) and the Division of Urology (Ms Seniuk and Dr Felsen), Department of Surgery, The New York (NY) Hospital–Cornell University Medical College.
Footnotes
Accepted for publication August 29, 1989.
Read before the Ninth Annual Meeting of the Surgical Infection Society, Denver, Colo, April 13, 1989.
Reprint requests to F2016, The New York Hospital, 525 E 68th St, New York, NY 10021 (Dr Moldawer).
CiteULike Connotea Del.icio.us Digg Reddit Technorati
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
 |
Pentoxifylline Inhibits Endotoxin-Induced NF-kappa B Activation and Associated Production of Proinflammatory Cytokines
Ji et al.
Annals of Clinical & Laboratory Science 2004;34:427-436.
ABSTRACT
| FULL TEXT
Effect of Ketamine on NF-kappa B Activity and TNF-alpha Production in Endotoxin-Treated Rats
Sun et al.
Annals of Clinical & Laboratory Science 2004;34:181-186.
ABSTRACT
| FULL TEXT
Administration of Progesterone After Trauma and Hemorrhagic Shock Prevents Hepatocellular Injury
Kuebler et al.
Arch Surg 2003;138:727-734.
ABSTRACT
| FULL TEXT
Revisiting the Role of Tumor Necrosis Factor {alpha} and the Response to Surgical Injury and Inflammation
Ksontini et al.
Arch Surg 1998;133:558-567.
ABSTRACT
| FULL TEXT
Mechanism of Hepatocellular Dysfunction During Early Sepsis: Key Role of Increased Gene Expression and Release of Proinflammatory Cytokines Tumor Necrosis Factor and Interleukin-6
Wang et al.
Arch Surg 1997;132:364-370.
ABSTRACT
Growth Hormone and Insulinlike Growth Factor I Enhance Host Defense in a Murine Sepsis Model
Inoue et al.
Arch Surg 1995;130:1115-1122.
ABSTRACT
Augmented Tumor Necrosis Factor Response to Lipopolysaccharide After Thermal Injury Is Regulated Posttranscriptionally
Minei et al.
Arch Surg 1994;129:1198-1203.
ABSTRACT
Bacterial Translocation Induces Procoagulant Activity in Tissue Macrophages: A Potential Mechanism for End-Organ Dysfunction
Sullivan et al.
Arch Surg 1991;126:586-590.
ABSTRACT
A.S.P.E.N. 1990 Research Workshop on Energy Metabolism
Matthews and Heymsfield
JPEN J Parenter Enteral Nutr 1991;15:3-14.
Hormonal Regulation of Protein Metabolism
Long and Lowry
JPEN J Parenter Enteral Nutr 1990;14:555-562.
Glutamine or Fiber Supplementation of a Defined Formula Diet: Impact on Bacterial Translocation, Tissue Composition, and Response to Endotoxin
Barber et al.
JPEN J Parenter Enteral Nutr 1990;14:335-343.
ABSTRACT
|