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 expression and function of breast regression protein 39 (BRP-39) in murine models of subacute cigarette smoke exposure and allergic airway inflammation. | Nikota et al. Respiratory Research 2011 12 39 http content 12 1 39 RESPIRATORY RESEARCH RESEARCH Open Access Differential expression and function of breast regression protein 39 BRP-39 in murine models of subacute cigarette smoke exposure and allergic airway inflammation 1 2 12 3 Jake K Nikota Fernando M Botelho Carla MT Bauer Manel Jordana Anthony J Coyle Alison A Humbles and Martin R Stampfli2 5 Abstract Background While the presence of the chitinase-like molecule YKL40 has been reported in COPD and asthma its relevance to inflammatory processes elicited by cigarette smoke and common environmental allergens such as house dust mite HDM is not well understood. The objective of the current study was to assess expression and function of BRP-39 the murine equivalent of YKL40 in a murine model of cigarette smoke-induced inflammation and contrast expression and function to a model of HDM-induced allergic airway inflammation. Methods CD1 C57BL 6 and BALB c mice were room air- or cigarette smoke-exposed for 4 days in a whole-body exposure system. In separate experiments BALB c mice were challenged with HDM extract once a day for 10 days. BRP-39 was assessed by ELISA and immunohistochemistry. IL-13 IL-1R1 IL-18 and BRP-39 knock out KO mice were utilized to assess the mechanism and relevance of BRP-39 in cigarette smoke- and HDM-induced airway inflammation. Results Cigarette smoke exposure elicited a robust induction of BRP-39 but not the catalytically active chitinase AMCase in lung epithelial cells and alveolar macrophages of all mouse strains tested. Both BRP-39 and AMCase were increased in lung tissue after HDM exposure. Examining smoke-exposed IL-1R1 IL-18 and IL-13 deficient mice BRP-39 induction was found to be IL-1 and not IL-18 or IL-13 dependent while induction of BRP-39 by HDM was independent of IL-1 and IL-13. Despite the importance of BRP-39 in cellular inflammation in HDM-induced airway inflammation BRP-39 was found to be redundant
