Inflammation as a target of minocycline: special interest in the regulation of inflammasome signaling

AbstractMinocycline is a wide-spectrum antibiotic derived from tetracycline. In addition to its anti-microbial activity, minocycline is known to possess several immunomodulatory and neuroprotective properties. Fewer severe side effects and more efficient tissue penetration make minocycline better than its parent tetracycline. Doxycycline competes with minocycline in improved biological half-life but minocycline becomes more rapidly absorbed in tissues than doxycycline. Due to its high lipid solubility, minocycline also crosses the blood-brain barrier easily, which increases its relevance in the treatment of diseases beyond the barriers. Inflammasomes are intracellular protein complexes which become primed via NF-kB and MAPK pathways, and activated by various PAMPs and DAMPs. In this article, we hypothese about the capability of minocycline to regulate inflammasomes as part of its anti-inflammatory activity. The hypothesis is based on the ability of minocycline to regulate signals essential to both the priming and the activation of inflammasome signaling