The modulation of reactive oxygen species production from human polymorphonuclear cells by Curdlan derivatives as Dectin-1 agonists/antagonists.

摘要: Abstract Reactive oxygen species (ROS) are well known to be cytotoxic and have been implicated in the etiology of a wide array human diseases including diabetes, neurodegenerative diseases, cancer also influence central cellular processes such as proliferation, apoptosis, senescence etc. If these pathological or degenerative conditions characterized by free radicals excess, reactive not eliminated, they can maintain destructive processes, already initiated at different levels. Understanding role ROS key mediators signaling cascades may provide various opportunities for pharmacological intervention. Toll-like receptors C-type lectin receptor class V--Dectin-1, members Pattern Recognition Receptors play an essential innate immune response against bacteria fungi respectively, contributing pathogens recognition, phagocytosis, production induction pro-inflammatory cytokines secretion. Using high performance chemiluminometric method, we studied action six Curdlan derivatives on release activated polymorphonuclear cells (PMNs) isolated from peripheral blood healthy donors. Our results demonstrated that containing sulfopropyl groups did activate PMNs ROS. These compounds blocked Dectin-1 were able inhibit co-operation between TLR-2. palmithoyl, carboxi-methyl increased TLR-2 level. Taking into account fact actively collaborate with modulate subsequent adaptive response, presume group palmithoyl/carboxi-methyl/sulfopropyl groups, possible antagonists/agonists, could signaling.