tailieunhanh - Báo cáo y học: "Inflammatory responses in epithelia: endotoxininduced IL-6 secretion and iNOS/NO production are differentially regulated in mouse mammary epithelial cells"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Inflammatory responses in epithelia: endotoxininduced IL-6 secretion and iNOS/NO production are differentially regulated in mouse mammary epithelial cells. | Maalouf et al. Journal of Inflammation 2010 7 58 http content 7 1 58 JOURNAL OF INFLAMMATION RESEARCH Open Access Inflammatory responses in epithelia endotoxin-induced IL-6 secretion and iNOS NO production are differentially regulated in mouse mammary epithelial cells Samar W Maalouf1 4 Rabih S Talhouk2 3 Floyd L Schanbacher1 Abstract Background IL-6 is a pro-inflammatory cytokine that signals via binding to a soluble or membrane bound receptor while nitric oxide NO an oxidative stress molecule diffuses through the cell membrane without a receptor. Both mediators signal through different mechanisms yet they are dependent on NFkB. We proposed that both mediators are co-induced and co-regulated in inflamed mammary epithelial cells. Methods SCp2 mammary epithelial cells were treated with bacterial endotoxin ET for different time periods and analyzed for induction of IL-6 secretion and NO production by ELISA and Griess reaction respectively. The expression of IL-6 and induced NO synthase INGS was assayed by real time PCR and or western immunoblots and the activation of NFkB was assayed by immunobinding assay. To investigate the role of mammary cell microenvironment cellsubstratum or interaction of mammary epithelial cell types critical to mammary development function and disease in modulation of the inflammatory response SCp2 cells were cultured with or without extracellular matrix EHS or in coculture with their myoepithelial counterpart SCg6 and assayed for ET-induced IL-6 and NO. Results Endotoxin induced NFkB activation at 1 h after ET application. IL-6 secretion and NO production were induced but with unexpected delay in expression of mRNA for INGS compared to IL-6. NF p65 activation was transient but NF p50 activation persisted longer. Selective inhibition ofNFkB activation by Wedelolactone reduced ET-induced expression of IL-6 mRNA and protein but not iNOS mRNA or NO production suggesting differences in IL-6 and iNOS .