Methylprednisolone inhibits neutrophil-endothelial cell interactions induced by interleukin-1beta under flow conditions

Life Sci. 1997;60(25):2341-7. doi: 10.1016/s0024-3205(97)00290-7.

Abstract

The effects of methylprednisolone (m-PSL) on IL-1beta-induced neutrophil-endothelial cell interactions, which are normally mediated by increased expression of both intercellular adhesion molecule-1 (ICAM-1) and E-selectin on endothelial cells, were examined using an in vitro flow system. Human neutrophilic polymorphonuclear leukocytes (PMN) were perfused at a shear stress of 1 dyne/cm2 on human umbilical vein endothelial cells (HUVEC) pretreated with IL-1beta (20 U/mL) for 4 hours. Many PMN adhered to IL-1-stimulated HUVEC and then migrated beneath endothelial cell monolayers. Treatment of HUVEC with m-PSL inhibited adherence and migration of PMN in a dose dependent manner. M-PSL also inhibited IL-1beta-induced upregulation of E-selectin and ICAM-1 on HUVEC in a dose dependent manner. These results suggest that m-PSL works as an anti-inflammatory agent through inhibiting PMN-endothelial cell interactions.

MeSH terms

  • Adult
  • Anti-Inflammatory Agents / pharmacology*
  • Cell Adhesion / drug effects
  • Cell Communication / drug effects*
  • Cell Survival / drug effects
  • E-Selectin / biosynthesis
  • Endothelium, Vascular / cytology*
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Humans
  • Intercellular Adhesion Molecule-1 / biosynthesis
  • Interleukin-1 / pharmacology*
  • Methylprednisolone / pharmacology*
  • Neutrophils / cytology*
  • Neutrophils / drug effects*

Substances

  • Anti-Inflammatory Agents
  • E-Selectin
  • Interleukin-1
  • Intercellular Adhesion Molecule-1
  • Methylprednisolone