nicotine modulates the release of inflammatory cytokines and expression of tlr2, tlr4 of cord blood mononuclear cells

The underlying mechanisms of how nicotine affects cord umbilical cells remain largely elusive. nicotine rapidly crosses the blood-brain barrier (10 to 20 s) and binds to nicotinic acetylcholine receptors (nachrs). nicotine considered as a major compound found in cigarette smoke and the mechanism of nicotine action in immune response is not well understood. cigarette smoke well known by activation of toll like receptors (tlrs) especially tlr4 and 9 which stimulates the immune response by induction of releases of cytokines mainly cxcl-8 which in turn triggers lungs reactions specially induction of neutrophils recruitments. in this study we isolated human umbilical mononuclear cells (ucbmc) from umbilical cord blood and exposed to the nicotine for detection any cytokines and tlrs modulation. we have found that nicotine (at concentration 0.01μm) induced release of tnf- and il-6 but not cxcl-8 production. besides we have shown that nicotine did not effect on tlr4 surface expression however up-regulated the tlr2 surface expression. moreover expression of cd11a and cxcr4 after nicotine incubation was upregulated as demonstrated by flow cytometry analysis, these data indicated that nicotine by stimulation of inflammatory cytokines induces immune response. the present study provides evidence that nicotine selectively regulates the release of cytokines and expression of tlrs. further studies are needed to exploring details of its effects and signaling.