Astrid Parenti1, Boris Indorato1, Sara Paccosi2. 1. Department of Health Sciences, Clinical Pharmacology and Oncology Section, University of Florence, Viale Pieraccini 6, 50139, Florence, Italy. 2. Department of Health Sciences, Clinical Pharmacology and Oncology Section, University of Florence, Viale Pieraccini 6, 50139, Florence, Italy. sara.paccosi@unifi.it.
Abstract
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.
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.
Authors: David Costa; Alexandra P Marques; Rui L Reis; José L F C Lima; Eduarda Fernandes Journal: Free Radic Biol Med Date: 2005-10-21 Impact factor: 7.376
Authors: Tammy Kielian; Nilufer Esen; Shuliang Liu; Nirmal K Phulwani; Mohsin M Syed; Napoleon Phillips; Koren Nishina; Ambrose L Cheung; Joseph D Schwartzman; Jorg J Ruhe Journal: Am J Pathol Date: 2007-08-23 Impact factor: 4.307