The effect of tobacco smoke on the metabolism and function of rat alveolar macrophages.
Alveolar macrophages harvested by bronchopulmonary lavage from rats exposed to tobacco smoke for 30 days ("smokers") showed alterations in oxidative metabolism, lactate production and phagocytosis of inert starch particles when compared with control macrophages. Phagocytosis of viable Staphylococcus aureus was unaffected by tobacco smoke. Glucose oxidation measured by conversion of glucose-1-14C to 14CO2 moderately affected while oxidation of glucose-6-14C to 14CO2 was not. Smokers routinely yielded fewer cells than controls, though these cells contained approximately 17% more protein than did controls. Opsonization of particles was not necessary for macrophages from either smoker or control animals to manifest a respiratory burst and increased superoxide and hydrogen peroxide release during phagocytosis. The glycolytic inhibitors, sodium fluoride and iodoacetamide, while effectively blocking glycolysis, did not inhibit phagocytosis by macrophages from either group. The results reported clearly distinguish alveolar macrophages from other phagocytic cells (peritoneal macrophages and polymorphonuclear leukocytes) and suggest a state of non-specific activation caused by exposure to tobacco smoke.
D000818:Animals; D002478:Cells, Cultured; D005947:Glucose / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D007773:Lactates / Q000096:biosynthesis; D008264:Macrophages / Q000502:physiology*; D010101:Oxygen Consumption; D010587:Phagocytosis; D010947:Plants, Toxic; D011650:Pulmonary Alveoli; D051381:Rats; D012906:Smoke; D013481:Superoxides / Q000378:metabolism; D014026:Nicotiana
D007773:Lactates; D012906:Smoke; D013481:Superoxides; D006861:Hydrogen Peroxide; D005947:Glucose