Abstract
Cachexia is a potentially lethal syndrome of unknown etiology characterized by anorexia, weight loss, and protein wasting that frequently complicates the treatment of chronic inflammation and cancer. Cachectin/TNF was isolated during the search for a humoral mediator of cachexia and found to stimulate the breakdown of energy stores from adipocytes and myocytes in vitro, but the chronic effects of the monokine in vivo are not known. Sublethal doses of recombinant human cachectin administered twice daily for 7-10 d caused cachexia in rats, as evidenced by reduced food intake, weight loss, and depletion of whole-body lipid and protein stores. Significant anemia is also observed and found to be the result of decreased red blood cell mass, not expanded plasma volume. Leukocytosis and histopathological evidence of tissue injury and inflammation are observed in several organs, including omentum, liver, spleen, and heart. These data suggest that the exposure of the normal host to cachectin is capable of inducing a pathophysiological syndrome of cachexia, anemia, and inflammation similar to that observed during inflammatory states or malignancy.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1211-1227 |
| Number of pages | 17 |
| Journal | Journal of Experimental Medicine |
| Volume | 167 |
| Issue number | 3 |
| State | Published - 1988 |
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ASJC Scopus subject areas
- Immunology
Cite this
Cachectin/tumor necrosis factor induces cachexia, anemia, and inflammation. / Tracey, K. J.; Wei, H.; Manogue, K. R.; Fong, Y.; Hesse, D. G.; Nguyen, H. T.; Kuo, G. C.; Beutler, B.; Cotran, R. S.; Cerami, A.; Lowry, S. F.
In: Journal of Experimental Medicine, Vol. 167, No. 3, 1988, p. 1211-1227.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cachectin/tumor necrosis factor induces cachexia, anemia, and inflammation
AU - Tracey, K. J.
AU - Wei, H.
AU - Manogue, K. R.
AU - Fong, Y.
AU - Hesse, D. G.
AU - Nguyen, H. T.
AU - Kuo, G. C.
AU - Beutler, B.
AU - Cotran, R. S.
AU - Cerami, A.
AU - Lowry, S. F.
PY - 1988
Y1 - 1988
N2 - Cachexia is a potentially lethal syndrome of unknown etiology characterized by anorexia, weight loss, and protein wasting that frequently complicates the treatment of chronic inflammation and cancer. Cachectin/TNF was isolated during the search for a humoral mediator of cachexia and found to stimulate the breakdown of energy stores from adipocytes and myocytes in vitro, but the chronic effects of the monokine in vivo are not known. Sublethal doses of recombinant human cachectin administered twice daily for 7-10 d caused cachexia in rats, as evidenced by reduced food intake, weight loss, and depletion of whole-body lipid and protein stores. Significant anemia is also observed and found to be the result of decreased red blood cell mass, not expanded plasma volume. Leukocytosis and histopathological evidence of tissue injury and inflammation are observed in several organs, including omentum, liver, spleen, and heart. These data suggest that the exposure of the normal host to cachectin is capable of inducing a pathophysiological syndrome of cachexia, anemia, and inflammation similar to that observed during inflammatory states or malignancy.
AB - Cachexia is a potentially lethal syndrome of unknown etiology characterized by anorexia, weight loss, and protein wasting that frequently complicates the treatment of chronic inflammation and cancer. Cachectin/TNF was isolated during the search for a humoral mediator of cachexia and found to stimulate the breakdown of energy stores from adipocytes and myocytes in vitro, but the chronic effects of the monokine in vivo are not known. Sublethal doses of recombinant human cachectin administered twice daily for 7-10 d caused cachexia in rats, as evidenced by reduced food intake, weight loss, and depletion of whole-body lipid and protein stores. Significant anemia is also observed and found to be the result of decreased red blood cell mass, not expanded plasma volume. Leukocytosis and histopathological evidence of tissue injury and inflammation are observed in several organs, including omentum, liver, spleen, and heart. These data suggest that the exposure of the normal host to cachectin is capable of inducing a pathophysiological syndrome of cachexia, anemia, and inflammation similar to that observed during inflammatory states or malignancy.
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UR - http://www.scopus.com/inward/citedby.url?scp=0023916786&partnerID=8YFLogxK
M3 - Article
C2 - 3351436
AN - SCOPUS:0023916786
VL - 167
SP - 1211
EP - 1227
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
SN - 0022-1007
IS - 3
ER -