tailieunhanh - Báo cáo y học: " Different regulation of cigarette smoke induced inflammation in upper versus lower airways"

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:Different regulation of cigarette smoke induced inflammation in upper versus lower airways. | Huvenne et al. Respiratory Research 2010 11 100 http content 11 1 100 RESPIRATORY RESEARCH RESEARCH Open Access Different regulation of cigarette smoke induced inflammation in upper versus lower airways 1 1 1 112 Wouter Huvenne Claudina A Pérez-Novo Lara Derycke Natalie De Ruyck Olga Krysko Tania Maes 2 2 2 2 2 1 Nele Pauwels Lander Robays Ken R Bracke Guy Joos Guy Brusselle Claus Bachert Abstract Background Cigarette smoke CS is known to initiate a cascade of mediator release and accumulation of immune and inflammatory cells in the lower airways. We investigated and compared the effects of CS on upper and lower airways in a mouse model of subacute and chronic CS exposure. Methods C57BL 6 mice were whole-body exposed to mainstream CS or air for 2 4 and 24 weeks. Bronchoalveolar lavage fluid BAL was obtained and tissue cryosections from nasal turbinates were stained for neutrophils and T cells. Furthermore we evaluated GCP-2 KC MCP-1 MIP-3a RORc IL-17 FoxP3 and TGF-P1 in nasal turbinates and lungs by RT-PCR. Results In both upper and lower airways subacute CS-exposure induced the expression of GCP-2 MCP-1 MIP-3a and resulted in a neutrophilic influx. However after chronic CS-exposure there was a significant downregulation of inflammation in the upper airways while on the contrary lower airway inflammation remained present. Whereas nasal FoxP3 mRNA levels already increased after 2 weeks lung FoxP3 mRNA increased only after 4 weeks suggesting that mechanisms to suppress inflammation occur earlier and are more efficient in nose than in lungs. Conclusions Altogether these data demonstrate that CS induced inflammation may be differently regulated in the upper versus lower airways in mice. Furthermore these data may help to identify new therapeutic targets in this disease model. Background Tobacco smoking can induce bronchial inflammation and structural changes and is one of the major causes of Chronic Obstructive Pulmonary Disease COPD which is .