Abstract
Chronic obstructive pulmonary disease (COPD) is currently the third leading cause of death globally and is characterized by airflow limitation that is progressive and not fully reversible. Cigarette smoking is the major cause of COPD. Fifty percent of deaths in the COPD population are due to a cardiovascular event and it is now recognised that COPD is a risk factor for stroke. Whether COPD increases stroke severity has not been explored. The aim of this study was to investigate whether functional and histological endpoints of stroke outcomes in mice after transient middle cerebral artery occlusion (tMCAo) were more severe in mice exposed to cigarette smoke (CS). 7-week-old male C57BL/6 mice were exposed to room air or CS generated from 9 cigarettes/day, 5 days/week for 2, 8 and 12 weeks. Following air or CS exposure, mice underwent tMCAO surgery with an ischaemic period of 30–40 min or sham surgery. Mice were euthanised 24 h following the induction of ischaemia and bronchoalveolar lavage fluid (BALF), lungs and brains collected. Mice exposed to CS for 2 weeks and subjected to a stroke had similar BALF macrophages to air-exposed and stroke mice. However, CS plus stroke mice had significantly more BALF total cells, neutrophils and lymphocytes than air plus stroke mice. Mice exposed to CS for 8 and 12 weeks had significantly greater BALF total cells, macrophages, neutrophils and lymphocytes than air-exposed mice, but stroke did not affect CS-induced BALF cellularity. Prior CS exposure did not worsen stroke-induced neurological deficit scores, reduced foregrip strength, infarct and oedema volumes. Collectively, we found that although CS exposure caused significant BALF inflammation, it did not worsen acute post-stroke outcomes in mice. This data suggests that while patients with COPD are at increased risk of stroke, it may not translate to COPD patients having more severe stroke outcomes.
Highlights
Chronic obstructive pulmonary disease (COPD) is currently the third leading cause of death globally [1, 2]
Mice exposed to cigarette smoke (CS) for 8 weeks had significantly greater bronchoalveolar lavage fluid (BALF) total cells, macrophages, neutrophils and lymphocytes (Fig 3 and S3 Fig) than air-exposed mice (P
Mice exposed to CS for 12 weeks had significantly greater BALF total cells, macrophages and neutrophils than air-exposed mice (P
Summary
Chronic obstructive pulmonary disease (COPD) is currently the third leading cause of death globally [1, 2]. Cigarette smoking is the major cause of COPD and accounts for more than 95% of cases in industrialized countries [3], but other environmental pollutants are important causes in developing countries [4]. COPD is characterized by an airway limitation. Cigarette smoke exposure and stroke that is usually progressive and not fully reversible [5], and is associated with a chronic and abnormal inflammatory response in the airways in response to noxious gases and particles [1]. COPD encompasses chronic obstructive bronchiolitis with fibrosis and obstruction of small airways, and emphysema with enlargement of airspaces and destruction of lung parenchyma, loss of lung elasticity, and closure of small airways. Most patients with COPD have all three pathological conditions (chronic obstructive bronchiolitis, emphysema and mucus plugging), but the relative extent of emphysema and obstructive bronchiolitis within individual patients
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