Minocycline affects human neutrophil respiratory burst and transendothelial migration

• Published in: Inflammation research Vol. 66; no. 2; pp. 107 - 109
• Main Authors: Parenti, Astrid, Indorato, Boris, Paccosi, Sara
• Format: Journal Article
• Language: English
• Published: Cham Springer International Publishing 01.02.2017; Springer Nature B.V
• Subjects: Allergology; Anti-Bacterial Agents - pharmacology; Anti-Inflammatory Agents - pharmacology; Biomedical and Life Sciences; Biomedicine; Cells, Cultured; Dermatology; Doxycycline - pharmacology; Humans; Immunology; Minocycline - pharmacology; Neurology; Neutrophils - drug effects; Neutrophils - metabolism; Neutrophils - physiology; Pharmacology/Toxicology; Reactive Oxygen Species - metabolism; Respiratory Burst - drug effects; Rheumatology; Short Communication; Transendothelial and Transepithelial Migration - drug effects; Minocycline; Inflammation; Transendothelial migration; ROS; Neutrophils
• ISSN: 1023-3830; 1420-908X; 1420-908X
• DOI: 10.1007/s00011-016-0999-x

Objective This study aimed at investigating the in vitro activity of minocycline and doxycycline on human polymorphonuclear (h-PMN) cell function. Methods 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. Results Minocycline (1–300 µM) concentration dependently and significantly inhibited oxidative burst of h-PMNs stimulated with 100 nM 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. 10–100 µM minocycline impaired PMN transendothelial migration, with maximal effect at 100 µM (42.5 ± 7 %, inhibition, n  = 5, P  < 0.001). Conclusions These results added new insight into anti-inflammatory effects of minocycline exerted on innate immune h-PMN cell function.