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Pathophysiologic alterations induced by tumor necrosis factor
1Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.
International Review of Experimental Pathology
|January 1, 1993
Summary
Tumor necrosis factor (TNF) can be toxic at high doses but may be essential for effective immune responses at low levels. Further research is needed to clarify TNF's role in organ injury during septic shock.
Area of Science:
- Immunology
- Pathophysiology
- Molecular Biology
Background:
- Tumor necrosis factor (TNF) is a peptide mediator known to cause toxicity and tissue damage in vivo at high concentrations.
- High levels of TNF during septic shock are detrimental, but its precise role in inflammation remains incompletely understood.
Purpose of the Study:
- To investigate the dual role of TNF in biological systems, considering its toxic effects at high doses and potential necessity at physiological levels.
- To elucidate the exact function of TNF in organ injury within the context of septic shock.
Main Methods:
- Review of existing laboratory data and published works on TNF's in vivo effects.
- Analysis of studies involving the inhibition of TNF using specific antibodies in bacterial infection models.
Main Results:
- High-dose, exogenous TNF (rHu-TNF) administration leads to toxicity.
- Inhibition of TNF in bacterial infection models has been shown to decrease survival rates.
- Low, physiological levels of TNF may be crucial for orchestrating effective immune responses.
Conclusions:
- TNF exhibits a dose-dependent effect, acting as a toxic agent at high concentrations and a potentially necessary mediator at low concentrations.
- Further investigation is required to fully define TNF's specific role in organ damage during septic shock.