Size and filterability of human and hamster pulmonary macrophages exposed to cigarette smoke

• Published in: Journal of leukocyte biology Vol. 40; no. 5; pp. 601 - 615
• Main Authors: C M Smith, 2nd, D P Tukey, R Boyd, D J Garlich, J Hoidal, C C Clawson
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Society for Leukocyte Biology 01.11.1986; Federation of American Societies for Experimental Biology
• Subjects: Animals; Biological and medical sciences; cell size; cigarette smoker; Cricetinae; Filtration; Humans; Macrophages - cytology; Macrophages - physiology; Macrophages - ultrastructure; Medical sciences; Microscopy, Electron; Pulmonary Alveoli - cytology; Smoking; Tobacco, tobacco smoking; Toxicology; Human; Deformability; Filtration; Respiratory disease; Lung; Rodentia; Tobacco smoking; Vertebrata; Tobacco; Mammalia; Pulmonary alveolus; Animal; Cell volume; Fumes; Hamster; Macrophage
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1002/jlb.40.5.601

Pulmonary alveolar macrophages (PAM) obtained from healthy human cigarette smokers generated greater pressure in filtration through small cylindrical pores than PAM from nonsmoking controls. A well standardized hamster smoking model was employed to study the structural basis for the impaired PAM filtration acompanying cigarette smoke exposure. Hamsters also demonstrated increased PAM filtration pressure through cylindrical pores less than half a cell diameter in size after inhalation of cigarette smoke, but not after exposure to vapor phase smoke that had been strained through a particle filter. Cigarette smoker PAM were equally filterable as control through larger diameter channels, and showed comparable improvements in filterability with cytochalasin B treatment. Altered PAM filtration was associated with the formation of characteristic cytoplasmic smoker inclusions, an increase in cell size, and loss of redundant, ruffled surface membrane. The study of smoker and control PAM separated into different sizes on the basis of variations in cell density suggested that discrepancies in cell size were insufficient to explain the filtration disparity. A loss of availability of surface membrane for deformation appeared to be the most important factor responsible for the impaired filtration.