Maintenance of radioresistant alveolar colony-forming cells in mice bearing pulmonary foreign-body inflammation after 89Sr-injection.
Murine pulmonary alveolar macrophages (PAMs) proliferate and form macrophage (M) colonies by cultures with granulocyte-macrophage (GM) colony-stimulating factor (GM-CSF). These alveolar colony-forming cells (AL-CFCs) are radioresistant. The present study was undertaken to investigate whether AL-CFCs are maintained or replaced by M-CFC sources outside the lung tissue in normal or inflammatory conditions. AL-CFCs were characterized in mice depleted of bone marrow cells and monocytes by a bone-seeking radiostrontium (89Sr), with or without the pulmonary inflammation induced by intratracheal instillation of foreign body Sephadex G50 beads (G50IT). No significant changes in the growth and radiosensitivity of AL-CFCs were observed in 89Sr-injected animals in which the circulating monocytes and CFC were less than 10% of 88Sr-injected control. The G50IT resulted in inflammatory cell exudation and about 1.5-fold increase of PAMs recovered in 88Sr-injected (control) animals, whereas no significant increase in PAMs was noted in 89Sr-injected animals. The plating efficiency of AL-CFCs per PAMs plated, was, however, almost comparable both in the groups of 88Sr/G50IT and 89Sr/G50IT. The survivals of irradiated AL-CFCs after G50IT were also not different from the normal steady state. These results indicate that radioresistant AL-CFCs are maintained in the lung, independently of recruited monocytes and other M-CFC sources.