The influence of nicotine on granulocytic differentiation – Inhibition of the oxidative burst and bacterial killing and increased matrix metalloproteinase-9 release-8

μg) of five day, DMSO-induced HL-60 cells without nicotine, or with 10M nicotine, or with 10M nicotine treatment, respectively. α7 nAChR-specific antibodies (Santa Cruz SC-5544) bound to protein bands exhibiting a relative molecular mass of 55.0 KDa in all lanes. Densitometric analysis () revealed that α7 nAChR-specific band intensities were significantly increased in the DMSO-treated samples, relative to promyelocytic cells (= 5, *< 0.05), but that this differentiation-associated increase α7 nAChR protein level was not influenced by nicotine exposure during differentiation in any statistically significant manner. α7 nAChR Immunofluorescence staining (×1000): Fixed five-day, DMSO-induced HL-60 cells were incubated with a polyclonal rabbit anti-α7 antibody (Santa Cruz SC-5544) before staining with a FITC-conjugated anti-rabbit antibody (Santa Cruz SC-2253). α7 nAChR-specific staining was evenly distributed across the cells. A similar cellular distribution of α7 nAChR was observed in promyelocytic cells (). Negative control for α7 nAChR Immunofluorescence staining (×1000).<p><b>Copyright information:</b></p><p>Taken from "The influence of nicotine on granulocytic differentiation – Inhibition of the oxidative burst and bacterial killing and increased matrix metalloproteinase-9 release"</p><p>http://www.biomedcentral.com/1471-2121/9/19</p><p>BMC Cell Biology 2008;9():19-19.</p><p>Published online 15 Apr 2008</p><p>PMCID:PMC2375863.</p><p>