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Tumor necrosis factor mediates endotoxic effects in mice
Infection and Immunity
|July 1, 1987
Summary
Recombinant human tumor necrosis factor (TNF) induced hypothermia and altered glucose and lactate levels in mice, mimicking endotoxin effects. These findings suggest TNF acts as an endogenous mediator of endotoxin responses.
Area of Science:
- Immunology
- Pathophysiology
Background:
- Bacterial endotoxins trigger significant physiological responses.
- Tumor necrosis factor (TNF) is a key cytokine involved in inflammatory processes.
Purpose of the Study:
- To investigate the pathophysiological effects of recombinant human tumor necrosis factor (TNF) in mice.
- To compare TNF-induced reactions with those caused by lipopolysaccharide (LPS).
Main Methods:
- Intravenous administration of recombinant human TNF to mice.
- Monitoring of physiological parameters including body temperature, plasma glucose, plasma lactate, blood hematocrit, and leukocyte counts.
Main Results:
- TNF induced a dose-dependent hypothermia, decreased plasma glucose, and increased plasma lactate levels.
- Increased blood hematocrit and transient leukopenia were observed post-TNF injection.
- No interleukin-1 activity was detected in TNF-treated animals.
Conclusions:
- The pathophysiological effects of TNF in mice closely resemble those induced by bacterial endotoxin.
- TNF may function as an endogenous mediator contributing to the systemic effects of endotoxin exposure.