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Platelet-activating factor promotes shear rate-dependent leukocyte adhesion in postcapillary venules
K Bienvenu1, J Russell, D N Granger
1Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130-3932.
Summary
Platelet-activating factor (PAF) increases leukocyte adhesion in cat mesenteric venules at reduced shear rates. This effect is mediated by the CD11/CD18 glycoprotein, not ICAM-1, highlighting a mechanism in microcirculation inflammation.
Area of Science:
- Microcirculation physiology
- Immunology
- Vascular biology
Background:
- Leukocyte adhesion in microcirculation is shear rate-dependent.
- Platelet-activating factor (PAF) is implicated in inflammatory processes.
Purpose of the Study:
- To investigate PAF's effect on shear rate-dependent leukocyte adhesion in cat mesenteric venules.
- To determine the role of CD11/CD18 and ICAM-1 glycoproteins in PAF-mediated leukocyte adhesion.
Main Methods:
- Leukocyte adhesion was studied in cat mesenteric venules under varying shear rates.
- Shear rates were manipulated by graded occlusion of the superior mesenteric artery.
- PAF was superfused, and the effects on rolling and adherent leukocytes were measured with and without specific monoclonal antibodies (MAbs) against CD11/CD18 and ICAM-1.
Main Results:
- PAF superfusion increased adherent leukocytes at basal and reduced shear rates, but not rolling leukocytes.
- A MAb against CD11/CD18 blocked the PAF-induced increase in adherent leukocytes.
- An ICAM-1 specific MAb did not affect PAF-induced leukocyte adhesion.
Conclusions:
- PAF enhances shear rate-dependent leukocyte adhesion in mesenteric venules.
- The CD11/CD18 glycoprotein plays a crucial role in PAF's pro-adhesive effect.
- PAF likely increases CD11/CD18 expression or activation on granulocytes, contributing to inflammatory responses.