Shock and tissue injury induced by recombinant human cachectin

Kevin J. Tracey, Bruce Beutler, Stephen F. Lowry, James Merryweather, Stephen Wolpe, Ian W. Milsark, Robert J. Hariri, Thomas J. Fahey, Alejandro Zentella, James D. Albert, G. Tom Shires, Anthony Cerami

Research output: Contribution to journalArticlepeer-review

2132 Scopus citations


Cachectin (tumor necrosis factor), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. Recombinant human cachectin was infused into rats in an effort to determine whether cachectin, by itself, can elicit the derangements of host physiology caused by administration of endotoxin. When administered in quantities similar to those produced endogenously in response to endotoxin, cachectin causes hypotension, metabolic acidosis, hemoconcentration, and death within minutes to hours, as a result of respiratory arrest. Hyperglycemia and hyperkalemia were also observed after infusion. At necropsy, diffuse pulmonary inflammation and hemorrhage were apparent on gross and histopathologic examination, along with ischemic and hemorrhagic lesions of the gastrointestinal tract, and acute renal tubular necrosis. Thus, it appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.

Original languageEnglish (US)
Pages (from-to)470-474
Number of pages5
Issue number4775
StatePublished - 1986

ASJC Scopus subject areas

  • General


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