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Platelet-activating factor augments tumor necrosis factor and procoagulant activity
R V Maier1, G B Hahnel, J R Fletcher
1Department of Surgery, University of Washington, Seattle.
The Journal of Surgical Research
|March 1, 1992
Summary
Platelet activating factor (PAF) amplifies the production of tumor necrosis factor (TNF) and procoagulant activity (PCA) by macrophages. This priming effect of PAF may explain its role in inflammatory conditions like sepsis.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Platelet activating factor (PAF) mimics physiological responses to endotoxemia and sepsis.
- Tumor necrosis factor (TNF) and procoagulant activity (PCA) are key inflammatory mediators produced by macrophages.
- The interaction between PAF and macrophage-derived TNF/PCA is not well understood.
Purpose of the Study:
- To investigate the relationship between PAF and the production of TNF and PCA by macrophages.
- To determine if PAF influences macrophage inflammatory mediator release in response to lipopolysaccharide (LPS).
Main Methods:
- Rabbit alveolar macrophages were treated in vitro with PAF alone or in combination with LPS.
- PAF concentrations and pre-treatment times were varied to assess dose- and time-dependent effects.
- Macrophage production of TNF and PCA was quantified.
Main Results:
- PAF alone did not affect macrophage PCA or TNF levels.
- Co-treatment with PAF and LPS dose-dependently enhanced PCA and TNF production (2-6 fold).
- Pre-treatment (priming) of macrophages with PAF prior to LPS stimulation resulted in an 8-9 fold increase in PCA and TNF.
Conclusions:
- PAF significantly enhances macrophage production of TNF and PCA when co-administered or used as a pre-treatment with LPS.
- These findings suggest that PAF's ability to prime macrophages contributes to its in vivo inflammatory effects, potentially exacerbating conditions like sepsis.