tailieunhanh - Báo cáo y học: " Expression of S100A8 correlates with inflammatory lung disease in congenic mice deficient of the cystic fibrosis transmembrane conductance regulator"

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: " Expression of S100A8 correlates with inflammatory lung disease in congenic mice deficient of the cystic fibrosis transmembrane conductance regulator. | Respiratory Research BioMed Central Research Open Access Expression of SI00A8 correlates with inflammatory lung disease in congenic mice deficient of the cystic fibrosis transmembrane conductance regulator Sam Tirkos1 Susan Newbigging2 Van Nguyen1 Mary Keet3 4 Cameron Ackerley5 Geraldine Kent5 and Richard F Rozmahel 1 3 4 Address Department of Pharmacology University of Toronto Toronto Ontario Canada 2Department of Pathobiology University of Guelph and Ontario Veterinary College Guelph Ontario Canada 3University of Western Ontario London Ontario Canada 4Lawson Health Research Institute London Ontario Canada and 5The Hospital for Sick Children Toronto ON Canada Email Sam Tirkos - Susan Newbigging - snewbigg@ Van Nguyen - Mary Keet - mkeet@ Cameron Ackerley - Geraldine Kent - gkent2@ Richard F Rozmahel - rrozmahe@ Corresponding author Published 29 March 2006 Received 18 October 2005 Respiratory Research2006 7 51 doi 1465-9921-7-51 Accepted 29 March 2006 This article is available from http content 7 1 51 2006Tirkos 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 Lung disease in cystic fibrosis CF patients is dominated by chronic inflammation with an early and inappropriate influx of neutrophils causing airway destruction. Congenic C57BL 6 CF mice develop lung inflammatory disease similar to that of patients. In contrast lungs of congenic BALB c CF mice remain unaffected. The basis of the neutrophil influx to the airways of CF patients and C57BL 6 mice and its precipitating factor s spontaneous or infection induced remains unclear. Methods The lungs of 20-day old