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Ethanol enhances leukocyte-endothelial cell interactions in mesenteric venules
P R Kvietys1, M A Perry, T S Gaginella
1Department of Physiology, Louisiana State University Medical Center, Shreveport 71130.
The American Journal of Physiology
|October 1, 1990
Summary
Ethanol promotes inflammation in vivo by increasing neutrophil adherence and migration, independent of hemodynamic changes. This effect relies on adhesive glycoproteins, not inflammatory mediators like PAF or LTB4.
Area of Science:
- Gastroenterology
- Immunology
- Toxicology
Background:
- Neutrophils are implicated in ethanol-induced gastric injury.
- In vitro studies suggest ethanol inhibits neutrophil functions.
- The in vivo proinflammatory effect of ethanol at clinical concentrations remains unclear.
Purpose of the Study:
- To determine if ethanol is proinflammatory in vivo at clinically relevant concentrations.
- To investigate the mechanisms of ethanol-induced neutrophil activation and migration.
Main Methods:
- Ethanol (0.2-4.0%) applied to cat mesentery.
- Intravital microscopy used to quantify neutrophil adherence and extravasation.
- Hemodynamic parameters measured; animals pretreated with anti-CD11/CD18 antibody, LTB4, or PAF antagonists.
Main Results:
- Ethanol caused a dose-dependent increase in neutrophil adherence and extravasation.
- Increased leukocyte-endothelial cell interactions were not due to hemodynamic alterations.
- Anti-CD11/CD18 antibody blocked ethanol-induced effects; LTB4 and PAF antagonists did not.
Conclusions:
- Ethanol is proinflammatory in vivo at concentrations relevant to acute alcohol intoxication.
- Ethanol-induced leukocyte adherence and extravasation depend on adhesive glycoproteins.
- PAF and LTB4 do not appear to mediate ethanol-induced leukocyte-endothelial interactions.