Báo cáo y học: " Differential regulation of CCL-11/eotaxin-1 and CXCL-8/IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle 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: " Differential regulation of CCL-11/eotaxin-1 and CXCL-8/IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle cells. | Respiratory Research BioMed Central Research Differential regulation of CCL-11 eotaxin-1 and CXCL-8 IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle cells Razao Issa 1 4 Rosalinda Sorrentino2 Maria B Sukkar1 Shiranee Sriskandan3 Kian Fan Chung1 and Jane A Mitchell 2 Address Experimental Studies Airway Disease Section National Heart Lung Institute Imperial College London London SW3 6LY UK 2Cardiothoracic Pharmacology Unit of Critical Care Medicine National Heart and Lung Institute Imperial College London London SW3 6LY UK 3Department of Infectious Diseases Immunity Division of Investigative Science Hammersmith Campus Imperial College London London W12 ONN UK and 4Novartis Horsham West Sussex RH12 5AB UK Email Razao Issa - razao_issa@ Rosalinda Sorrentino - Maria B Sukkar - Shiranee Sriskandan - Kian Fan Chung - Jane A Mitchell - Corresponding authors Open Access Published I April 2008 Received 29 June 2007 Respiratory Research 2008 9 30 doi 1465-9921-9-30 Accepted 1 April 2008 This article is available from http content 9 1 30 2008 Issa 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 Bacterial infections are a cause of exacerbation of airway disease. Airway smooth muscle cells ASMC are a source of inflammatory cytokines chemokines that may propagate local airway inflammatory responses. We hypothesize that bacteria and bacterial products could induce cytokine chemokine release from ASMC. Methods Human ASMC were grown in culture and treated with whole bacteria or pathogen associated molecular

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