tailieunhanh - Báo cáo y học: "Selective regulation of MAP kinases and Chemokine expression after ligation of ICAM-1 on human airway epithelial cells"

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: "Selective regulation of MAP kinases and Chemokine expression after ligation of ICAM-1 on human airway epithelial cells. | Respiratory Research BioMed Central Research Open Access Selective regulation of MAP kinases and Chemokine expression after ligation of ICAM-1 on human airway epithelial cells Thomas M Krunkosky and Carla L Jarrett Address Department of Anatomy Radiology College of Veterinary Medicine University of Georgia Athens GA 30602 USA Email Thomas M Krunkosky - tmkrunko@ Carla L Jarrett - cjarrett@ Corresponding author Published 23 January 2006 Received 28 April 2005 Respiratory Research 2006 7 12 doi 1465-9921-7-12 Accepted 23 January 2006 This article is available from http content 7 1 12 2006 Krunkosky and Jarrett 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 Intercellular adhesion molecule I ICAM-I is an immunoglobulin-like cell adhesion molecule expressed on the surface of multiple cell types including airway epithelial cells. It has been documented that cross-linking ICAM-1 on the surface of leukocytes results in changes in cellular function through outside-inside signaling however the effect of cross-linking ICAM-1 on the surface of airway epithelial cells is currently unknown. The objective of this study was to investigate whether or not cross-linking ICAM-1 on the surface of airway epithelial cells phosphorylated MAP kinases or stimulated chemokine expression and secretion. Methods The human lung adenocarcinoma A549 cells and primary cultures of normal human bronchial epithelial NHBE cells were used in these studies. To increase ICAM-1 surface expression cultures were stimulated with TNFa to enhance ICAM-1 surface expression. Following ICAM-1 upregulation ICAM-1 was ligated with a murine anti-human ICAM-1 antibody and subsequently cross-linked with