Minocycline affects human neutrophil respiratory burst and transendothelial migration.

Abstract

This study aimed at investigating the in vitro activity of minocycline and doxycycline on human polymorphonuclear (h-PMN) cell function. h-PMNs were isolated from whole venous blood of healthy subjects; PMN oxidative burst was measured by monitoring ROS-induced oxidation of luminol and transendothelial migration was studied by measuring PMN migration through a monolayer of human umbilical vein endothelial cells. Differences between multiple groups were determined by ANOVA followed by Tukey's multiple comparison test; Student's t test for unpaired data for two groups. Minocycline (1-300µM) concentration dependently and significantly inhibited oxidative burst of h-PMNs stimulated with 100nM fMLP. Ten micromolar concentrations, which are superimposable to C max following a standard oral dose of minocycline, promoted a 29.8±4% inhibition of respiratory burst (P<0.001; n=6). Doxycycline inhibited ROS production with a lesser extent and at higher concentrations. 10-100µM minocycline impaired PMN transendothelial migration, with maximal effect at 100µM (42.5±7%, inhibition, n=5, P<0.001). These results added new insight into anti-inflammatory effects of minocycline exerted on innate immune h-PMN cell function.