Endothelial cells potentiate phagocytic killing by macrophages via platelet-activating factor release

Tetsuhiro Owaki, Avedis Meneshian, Kosei Maemura, Sonshin Takao, Dajie Wang, Katherine C. Fuh, Gregory B. Bulkley, Andrew S. Klein

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


The immunomodulatory function of endothelial cells (EC) includes the initiation of leukocyte margination, diapedesis, and activation through the upregulation of various cell surface-associated molecules. However, the effect that EC have on the phagocytic function of neighboring monocytes and macrophages is less well described. To address this issue, microvascular EC were cocultured with murine peritoneal macrophages, first in direct contact, then in a noncontact coculture system, and macrophage phagocytosis and phagocytic killing were assessed. The presence of increasing concentrations of EC resulted in a dose-dependent increase in macrophage phagocytic killing. This stimulatory effect was inhibited in a dose-dependent manner by the pretreatment of macrophage/EC cocultures with WEB-2086 or CV-6209, specific platelet-activating factor (PAF)-receptor antagonists, but not by anti-tumor necrosis factor-α, anti-interleukin (IL)-1α, or anti-IL-1β. Furthermore, the effect was reproduced in the absence of EC by the exogenous administration of nanomolar concentrations of PAF. Microvascular EC potentiate macrophage phagocytic killing via the release of a soluble signal; PAF appears to be an important component of that signal.

Original languageEnglish
Pages (from-to)H269-H276
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 47-1
StatePublished - Jan 2000


  • Cytokines
  • Endothelium
  • Immunomodulation
  • Phagocytosis


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