Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" Differentiated transplant derived airway epithelial cell cytokine secretion is not regulated by cyclosporine. | Floreth et al. Respiratory Research 2011 12 44 http content 12 1 44 RESPIRATORY RESEARCH RESEARCH Open Access Differentiated transplant derived airway epithelial cell cytokine secretion is not regulated by cyclosporine Timothy Floreth Eric Sternt Yingli Tu Randi Stern Edward R Garrity Jr Sangeeta M Bhorade and Steven R White Abstract Background While lung transplantation is an increasingly utilized therapy for advanced lung diseases chronic rejection in the form of Bronchiolitis Obliterans Syndrome BOS continues to result in significant allograft dysfunction and patient mortality. Despite correlation of clinical events with eventual development of BOS the causative pathophysiology remains unknown. Airway epithelial cells within the region of inflammation and fibrosis associated with BOS may have a participatory role. Methods Transplant derived airway epithelial cells differentiated in air liquid interface culture were treated with IL-1P and or cyclosporine after which secretion of cytokines and growth factor and gene expression for markers of epithelial to mesenchymal transition were analyzed. Results Secretion of IL-6 IL-8 and TNF-a but not TGF-P1 was increased by IL-1P stimulation. In contrast to previous studies using epithelial cells grown in submersion culture treatment of differentiated cells in ALI culture with cyclosporine did not elicit cytokine or growth factor secretion and did not alter IL-6 IL-8 or TNF-a production in response to IL-1P treatment. Neither IL-1P nor cyclosporine elicited expression of markers of the epithelial to mesenchymal transition E-cadherin EDN-fibronectin and a-smooth muscle actin. Conclusion Transplant derived differentiated airway epithelial cell IL-6 IL-8 and TNF-a secretion is not regulated by cyclosporine in vitro these cells thus may participate in local inflammatory responses in the setting of immunosuppression. Further treatment with IL-1P did not elicit gene expression of markers of epithelial to
