Exposure to environmental tobacco smoke (ETS) is known to contribute to and exacerbate inflammatory diseases of the lung such as chronic obstructive pulmonary disease (COPD) and asthma. The effect of ETS on angiogenesis and leukocyte recruitment, both of which promote lung inflammation, was investigated using lung tissue from mice exposed to aged and diluted sidestream cigarette smoke or fresh air for 12 weeks and transplanted into dorsal skin-fold chambers in nude mice. Lung tissue from mice exposed to cigarette smoke for 12 weeks exhibited significantly increased vascular density (angiogenesis) associated with selectin-mediated increased intravascular leukocyte rolling and adhesion compared to fresh air-exposed lung tissue by intravital microscopy. Further, neutrophils from nicotine-exposed mice displayed significantly increased rolling and adhesion compared to control neutrophils in microvessels of nicotine-exposed lungs versus control lung microvessels, suggesting that nicotine in cigarette smoke can augment leukocyte-endothelial interactions. ETS-induced angiogenesis and leukocyte trafficking may play a key role in airway recruitment of inflammatory cells in ETS-associated disorders such as COPD bronchitis or asthma.
Bibliographical noteFunding Information:
Received 18 August 2008; accepted 3 September 2008. This study was supported by grants from the California Tobacco-related Disease Research Program (10 RT-0171) and National Institutes of Health (AI 35796) to P.S. Address correspondence to P. Sriramarao, PhD, Department of Veterinary and Biomedical Sciences and Department of Medicine, University of Minnesota, St. Paul, MN 55108, USA. E-mail: firstname.lastname@example.org
- Environmental tobacco smoke
- Leukocyte trafficking
- Lung angiogenesis