Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Emphysema is associated with increased inflammation in lungs of atherosclerosis-prone mice by cigarette smoke: implications in comorbidities of COPD. | Arunachalam et al. Journal of Inflammation 2010 7 34 http content 7 1 34 JOURNAL OF INFLAMMATION RESEARCH Open Access Emphysema is associated with increased inflammation in lungs of atherosclerosis-prone mice by cigarette smoke implications in comorbidities of COPD Gnanapragasam Arunachalam Isaac K Sundar Jae-woong Hwang Hongwei Yao Irfan Rahman Abstract Background Chronic obstructive pulmonary disease is associated with numerous vascular effects including endothelial dysfunction arterial stiffness and atherogenesis. It is also known that a decline in lung function is associated with increased cardiovascular comorbidity in smokers. The mechanism of this cardiopulmonary dual risk by cigarette smoke CS is not known. We studied the molecular mechanisms involved in development of emphysema in atherosclerosis-prone apolipoprotein E-deficient ApoE- - mice in response to CS exposure. Methods Adult male and female wild-type WT mice of genetic background C57BL 6J and ApoE- - mice were exposed to CS and lung inflammatory responses oxidative stress lipid peroxidation products mechanical properties as well as airspace enlargement were assessed. Results and Discussion The lungs of ApoE- - mice showed augmented inflammatory response and increased oxidative stress with development of distal airspace enlargement which was accompanied with decline in lung function. Interestingly the levels and activities of matrix metalloproteinases MMP-9 and MMP-12 were increased whereas the level of eNOS was decreased in lungs of CS-exposed ApoE- - mice as compared to air-exposed ApoE- -mice or CS-exposed WT mice. Conclusion These findings suggest that CS causes premature emphysema and a decline of lung function in mice susceptible to cardiovascular abnormalities via abnormal lung inflammation increased oxidative stress and alterations in levels of MMPs and eNOS. Background Chronic obstructive pulmonary disease COPD is characterized by chronic airflow limitation .