Methylprednisolone inhibits neutrophil-endothelial cell interactions induced by interleukin-1beta under flow conditions.
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.
Yoshida
N
N
First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kamigyo-ku, Japan.
Yoshikawa
T
T
Nakamura
Y
Y
Takenaka
S
S
Sakamoto
K
K
Manabe
H
H
Nakagawa
S
S
Kondo
M
M
D000328:Adult; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002448:Cell Adhesion / Q000187:drug effects; D002450:Cell Communication / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D019040:E-Selectin / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007375:Interleukin-1 / Q000494:pharmacology*; D008775:Methylprednisolone / Q000494:pharmacology*; D009504:Neutrophils / Q000166:cytology* / Q000187:drug effects*
D000893:Anti-Inflammatory Agents; D019040:E-Selectin; D007375:Interleukin-1; D018799:Intercellular Adhesion Molecule-1; D008775:Methylprednisolone