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:Alcohol reversibly disrupts TNF-α/TACE interactions in the cell membrane. | Respiratory Research BioMed Central Research Open Access Alcohol reversibly disrupts TNF-a TACE interactions in the cell membrane Kejing Song1 Xue-Jun Zhao2 Luis Marrero1 Peter Oliver1 Steve Nelson1 and Jay K Kolls 2 Address 1LSUHSC Gene Therapy Program and the LSUHSC Alcohol Research Center LSU Health Sciences Center CSRB Rm. 601 533 Bolivar St. New Orleans LA 70112 USA and 2Children s Hospital of Pittsburgh University of Pittsburgh Rm. 3765 3705 Fifth Ave. Pittsburgh PA 15213 USA Email Kejing Song - ksong@ Xue-Jun Zhao - Luis Marrero - lmarre@ Peter Oliver - polive@ Steve Nelson - snelso1@ Jay K Kolls - Corresponding author Published 24 October 2005 Received 14 July 2005 Respiratory Research 2005 6 123 doi 1465-9921-6-123 Accepted 24 October 2005 This article is available from http content 6 1 123 2005 Song et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Alcohol abuse has long been known to adversely affect innate and adaptive immune responses and pre-dispose to infections. One cellular mechanism responsible for this effect is alcohol-induced suppression of TNF-a TNF by mononuclear phagocytes. We have previously shown that alcohol in part inhibits TNF-a processing by TNF converting enzyme TACE in human monocytes. We hypothesized that the chain length of the alcohol is critical for post-transcriptional suppression of TNF secretion. Methods Due to the complex transcriptional and post-transcriptional regulation of TNF in macrophages to specifically study TNF processing at the cell membrane we performed transient transfections of A549 cells with the TNF cDNA driven by the heterologous CMV .
