tailieunhanh - Báo cáo y học: "Smoking and nicotine exposure delay development of collagen-induced arthritis in mice"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Smoking and nicotine exposure delay development of collagen-induced arthritis in mice. | Available online http content 11 3 R88 Research article Smoking and nicotine exposure delay development of collagen-induced arthritis in mice Sofia S Lindblad1 Piotr Mydel1 2 Ing-Marie Jonsson1 Robert M Senior2 Andrej Tarkowski1 and Maria Bokarewa1 1 Department of Rheumatology and Inflammation Research University of Gothenburg Sahlgrenska University Hospital Guldhedsgatan 10 Goteborg S-41346 Sweden 2Department of Medicine Division of Pulmonary and Critical Care Medicine Washington University 660 S. Euclid Avenue Campus Box 8052 St. Louis Missouri 63110 USA Contributed equally Corresponding author Sofia S Lindblad Received 25 Feb 2009 Revisions requested 30 Mar 2009 Revisions received 8 Jun 2009 Accepted 11 Jun 2009 Published 11 Jun 2009 Arthritis Research Therapy 2009 11 R88 doi ar2728 This article is online at http content 11 3 R88 2009 Lindblad 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. Open Access Abstract Introduction Recent epidemiologic studies have implicated smoking as an environmental risk factor for the development of rheumatoid arthritis RA . The aim of the present study is the evaluation of the role of cigarette smoke CS in the pathogenesis of collagen-induced arthritis in mice. Methods DBA 1 mice exposed to CS for 16 weeks n 25 and mice exposed to nicotine in drinking water n 10 were immunized with collagen type II CII . Severity of arthritis was evaluated clinically and morphologically and compared with control mice n 35 . Intensity of inflammation was evaluated by serum IL-6 and TNF-a levels. Additionally antibody response to CII anti-CII and citrullinated peptides aCCP was measured. Results Clinical evaluation of .

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