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Updated: Jun 21, 2026
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Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
Published on: April 9, 2018
Platelet-activating factor priming of inflammatory cell activity requires cellular adherence
Joseph Cuschieri1, David Gourlay, Eileen Bulger
1Department of Surgery, University of Cincinnati, Ohio 45267-0558, USA.
Surgery
|September 10, 2002
Summary
Platelet-activating factor (PAF) primes inflammatory cells only when they are adhered to tissues. This cellular adherence is crucial for PAF
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Platelet-activating factor (PAF) primes tissue-fixed inflammatory cells but not circulating ones.
- Cellular adherence involves cytoskeletal reorganization, vital for inflammatory cell function.
Purpose of the Study:
- To investigate the role of cellular adherence in Platelet-activating factor (PAF) priming of inflammatory cells.
Main Methods:
- Differentiated THP-1 cells were cultured under adherent and nonadherent conditions.
- Cells were pretreated with PAF, followed by endotoxin stimulation.
- Western blot and ELISA were used to analyze signaling cascades and cytokine production.
Main Results:
- Cellular adherence significantly enhanced endotoxin-induced activation of inflammatory signaling pathways (IL-1 kinase, ERK1/2, p38) and NF-κB translocation.
- PAF induced priming only in adherent cells, marked by increased IL-1 kinase, ERK1/2 activity, NF-κB translocation, and production of IL-6, IL-8, and TNF-α.
- PAF did not significantly affect p38 activity or IL-10 production.
Conclusions:
- Platelet-activating factor (PAF) primes mononuclear cells by enhancing Toll-mediated signaling exclusively under adherent conditions.
- PAF-induced priming in vivo is likely restricted to stimulated adherent inflammatory cells at tissue sites, with minimal systemic effects on circulating cells.
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