Báo cáo y học: " Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus Enterotoxin B in mice"

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: " Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus Enterotoxin B in mice. | Huvenne et al. Respiratory Research 2011 12 69 http content 12 1 69 RESPIRATORY RESEARCH RESEARCH Open Access Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus Enterotoxin B in mice A r ii I tor I Il i onno11 RI Ion A I annbanbor 2 t Tllna ICn cbm1 k on R Rranbo2 Tino Romoor3 Rotor A I lollinnc4 vvuutcl HUvcHHc Ellen I A LdlllKdCKcl ga l cH R DldCIXe line DcHUUl Peter W Hennigs Guy G Drusselle2 Guy F Joos2 Claus Dachert1 and Tania Maes2 Abstract Background Cigarette smoke CS is a major risk factor for the development of COPD. CS exposure is associated with an increased risk of bacterial colonization and respiratory tract infection because of suppressed antibacterial activities of the immune system and delayed clearance of microbial agents from the lungs. Colonization with Staphylococcus aureus results in release of virulent enterotoxins with superantigen activity which causes T cell activation. Objective To study the effect of Staphylococcus aureus enterotoxin D SED on CS-induced inflammation in a mouse model of COPD. Methods C57 Dl6 mice were exposed to CS or air for 4 weeks 5 cigarettes exposure 4x day 5 days week . Endonasal SED 10 pg ml or saline was concomitantly applied starting from week 3 on alternate days. 24 h after the last CS and SED exposure mice were sacrificed and bronchoalveolar lavage DAL fluid and lung tissue were collected. Results Combined exposure to CS and SED resulted in a raised number of lymphocytes and neutrophils in DAL as well as increased numbers of CD8 T lymphocytes and granulocytes in lung tissue compared to sole CS or SED exposure. Moreover concomitant CS SED exposure induced both IL-13 mRNA expression in lungs and goblet cell hyperplasia in the airway wall. In addition combined CS SED exposure stimulated the formation of dense organized aggregates of D- and T- lymphocytes in lungs as well as significant higher CXCL-13 protein mRNA and CCL19 mRNA levels in lungs.

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