Weight loss associated with an endotoxin-induced mediator from peritoneal macrophages: The role of cachectin (tumor necrosis factor)

Anthony Cerami, Yoshihiko Ikeda, Nguyen Le Trang, Peter J. Hotez, Bruce Beutler

Research output: Contribution to journalArticle

150 Scopus citations


Endotoxin-induced cells of the reticuloendothelial system were shown to produce mediator(s) that evoke a state of cachexia in recipient animals. The factor(s) responsible were assayed in endotoxin-resistant (C3H/HeJ) mice, which were injected with dialyzed conditioned medium obtained from lipopolysaccharide-induced peritoneal macrophages. The mice exhibited weight loss and anorexia, and they died if sufficient quantities of medium were administered. The syndrome was reversible if injections were discontinued. Endotoxin alone did not produce this effect, and no gross pathologic lesions were discernable in the treated animals. In this model system, cachexia appears to result from the action of soluble macromolecules produced by activated macrophages in vitro. Cachectin (murine tumor necrosis factor) is thought to play a central role in this phenomenon.

Original languageEnglish (US)
Pages (from-to)173-177
Number of pages5
JournalImmunology Letters
Issue number3-4
StatePublished - 1985



  • cachectin
  • endotoxin
  • tumor necrosis factor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this