PHAGOCYTOSIS BY DIVIDING AND NONDIVIDING MURINE ALVEOLAR MACROPHAGES

Abstract

Mice were exposed to an aerosol of fluorescent polystyrene microspheres with nominal diameter 0.89 mum. At 1, 5, 20, and 156 days after exposure, groups of mice were injected with 5-bromo-2'-deoxyuridine (BrdU) and killed 1 h later. The lungs were excised and lavaged with physiological saline to recover free cells. Cytospin slides were prepared, some of which were stained with May-Grunwald/Giemsa and others with a monoclonal antibody for BrdU. At each time point the phagocytic indices and particle/cell profiles were determined for alveolar macrophages (AM) in S-phase and for nondividing cells. The phagocytic indices and particle/cell profiles of the two populations did not differ significantly, showing that the phagocytic competence of AM in S-phase is the same as that of AM in other stages of the cell cycle. Changes in particle/cell profiles were measured during the study, and a simple model was devised that gave good agreement with the values observed at different times. This suggests that a daily loss of 2% of the AM population can be balanced by AM proliferation in situ without invoking a monocyte precursor. that monocytes in the lung capillaries enter the alveoli differentiate into macrophages. Only after this maturation the resulting cells acquire the specific metabolic, functional, properties of AM (Masse et al., 1977). of the processes by which the alveolar macrophage population has been published by Fritsch and Masse (1992). In the 2.5% of the AM population is lost daily to the upper respiratory daily production of AM by proliferation in situ more than offsets but the total daily loss of AM when cell death is taken into amounts to about 8-9%. Fritsch and Masse suggested that the shortfall required for homeostasis is made up by monocyte precursors