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Related Experiment Videos

Physiological responses to cachectin.

K J Tracey1, S F Lowry, A Cerami

  • 1Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.

Ciba Foundation Symposium
|January 1, 1987
PubMed
Summary
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Scientists identified a macrophage protein, cachectin, now known as tumor necrosis factor (TNF), responsible for cachexia and shock. This protein plays a key role in the body's response to infection and inflammation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pathophysiology

Background:

  • Mammals exhibit catabolic states, weight loss, and cachexia during infections or with tumors.
  • The precise mechanisms driving these wasting conditions, particularly in parasitic diseases, remain largely unknown.
  • Macrophage-derived proteins are implicated in systemic catabolic responses.

Purpose of the Study:

  • To identify and characterize the molecule responsible for cachexia and shock.
  • To elucidate the role of macrophage-derived proteins in pathological conditions.
  • To investigate the function and regulation of cachectin.

Main Methods:

  • Isolation and characterization of a macrophage protein, termed cachectin.
  • Investigating cachectin's response to endotoxin and other microbial products.

Related Experiment Videos

  • Studying cachectin's effects on adipocytes, including mRNA production and enzyme activity.
  • Comparing cachectin's properties with known cytokines like TNF and IL-1.

    • Main Results:

    • Cachectin was identified as a key mediator of cachexia and shock.
    • Cachectin production is induced by endotoxin and microbial products.
    • Cachectin suppresses anabolic enzymes in adipocytes by inhibiting mRNA.
    • Cachectin was found to be identical to tumor necrosis factor (TNF).
    • Cachectin induces fever, anorexia, and lethal shock in experimental animals.

    Conclusions:

    • Cachectin (TNF) is a crucial mediator in the pathogenesis of cachexia and endotoxin-induced shock.
    • While low levels may aid pathogen clearance, excessive cachectin production leads to detrimental catabolic stress.
    • This discovery expands the understanding of cachectin's diverse biological roles and its involvement in disease.