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:" Protease-activated receptor 2 activation of myeloid dendritic cells regulates allergic airway inflammation. | Lewkowich et al. Respiratory Research 2011 12 122 http content 12 1 122 RESPIRATORY RESEARCH RESEARCH Open Access Protease-activated receptor 2 activation of myeloid dendritic cells regulates allergic airway inflammation Ian P Lewkowich1 Scottie B Day1 John R Ledford1 Ping Zhou1 Krista Dienger1 Marsha Wills-Karp1 2 and Kristen Page1 2 Abstract Background A common characteristic of allergens is that they contain proteases that can activate protease-activated receptor PAR-2 however the mechanism by which PAR-2 regulates allergic airway inflammation is unclear. Methods Mice wild type and PAR-2-deficient were sensitized using German cockroach GC feces frass the isolated protease from GC frass or through adoptive transfer of GC frass-treated bone marrow-derived dendritic cells BMDC and measurements of airway inflammation cellular infiltration cytokine expression and mucin production serum IgE levels and airway hyperresponsiveness AHR were assessed. BMDC were cultured treated with GC frass and assessed for cytokine production. PAR-2 expression on pulmonary mDCs was determined by flow cytometry. Results Exposure to GC frass induced AHR and airway inflammation in wild type mice however PAR-2-deficient mice had significantly attenuated responses. To directly investigate the role of the protease we isolated the protease from GC frass and administered the endotoxin-free protease into the airways of mice in the presence of OVA. GC frass proteases were sufficient to promote the development of AHR serum IgE and Th2 cytokine production. PAR-2 expression on mDC was upregulated following GC frass exposure but the presence of a functional PAR-2 did not alter antigen uptake. To determine if PAR-2 activation led to differential cytokine production we cultured BMDC in the presence of GM-CSF and treated these cells ex vivo with GC frass. PAR-2-deficient BMDC released significantly less IL-6 IL-23 and TNFa compared to BMDC from wild type mice suggesting PAR-2 .
