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Metabolic responses to cachectin/TNF. A brief review
1Division of Neurosurgery, New York Hospital-Cornell Medical Center, New York 10021.
Annals of the New York Academy of Sciences
|January 1, 1990
Summary
Tumor necrosis factor-alpha (TNF-alpha) is a key cytokine in cachexia and septic shock. Inhibiting TNF-alpha protects against lethal shock, highlighting its pivotal role in inflammatory cascades.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Cachectin/tumor necrosis factor (TNF-alpha) is a macrophage-secreted cytokine.
- Initially identified as a factor suppressing lipoprotein lipase in cachectic animals.
- Proven identical to TNF-alpha through recombinant human cachectin biosynthesis.
Purpose of the Study:
- To elucidate the diverse biological activities of cachectin/TNF.
- To investigate its role in cellular cachexia and catabolic responses.
- To determine its involvement in septic shock and potential therapeutic inhibition.
Main Methods:
- Investigated cachectin/TNF effects on adipocytes and skeletal muscle cells in vitro.
- Observed effects of chronic and acute systemic cachectin/TNF exposure.
- Utilized monoclonal anti-cachectin antibodies in baboon models of Gram-negative bacteremia.
Main Results:
- Cachectin/TNF suppresses lipogenic enzymes and induces catabolic responses in cells.
- Chronic exposure leads to cachexia syndrome; acute exposure causes lethal shock.
- Monoclonal antibody inhibition protected baboons from septic shock and mortality.
Conclusions:
- Cachectin/TNF is a pivotal factor mediating septic shock.
- It plays a role in cellular cachexia and catabolic processes.
- Further research into its immunological and metabolic effects is crucial for understanding infection and inflammation.