Tobacco smoke and the pulmonary alveolar macrophage.
Our results indicate that tobacco smoke exposure to varying duration causes morphological, biochemical and functional alterations in pulmonary alveolar macrophages. The results of these changes is a population of alveolar macrophages made up of larger cells, with a reduced nucleus-cytoplasmic ratio, which are heavily loaded with heterolysosomes containing lipid. Though their fractional complement of mitochondria remains the same, an increase in the inner mitochondrial membrane surface area may be related to an enhanced oxidative metabolism. The cell is biochemically activated particularly following chronic exposure and is functionally impaired with respect to phagocytosis.
D000818:Animals; D005947:Glucose / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D008168:Lung / Q000166:cytology; D008264:Macrophages / Q000503:physiopathology* / Q000648:ultrastructure; D008297:Male; D010101:Oxygen Consumption; D010587:Phagocytosis; D051381:Rats; D012907:Smoking / Q000503:physiopathology*; D013211:Staphylococcus aureus; D013347:Subcellular Fractions; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors
D013481:Superoxides; D006861:Hydrogen Peroxide; D005947:Glucose