Adaptive responses of the pulmonary macrophagic system to carbon. II. Morphologic studies.
The increased output of alveolar macrophages in response to a heavy load of particulate material is well known but the relationship of this cellular outpouring to the precise location of the particles is not clear. The present study utilized an overload situation in which 4 mg. of carbon were instilled into the lungs of mice; the sequential cellular events were correlated with the patterns of carbon transport over a 28-day period using light and electron microscopy. At 12 hours some free carbon crossed the type 1 cells to reach the interstitium; later it was observed in peribronchial and perivascular interstitial cells. In the alveoli, free macrophages were loaded with carbon but passage of these cells from airways to interstitium was never observed. The early increase in macrophagic output was related to monocytic migration from small pulmonary vessels. This initial cellular efflux may be a nonspecific inflammatory response that is possibly due to release of a chemotactic factor by the interaction of carbon with the type 1 cells. Maintenance of the large number of free macrophages appeared to be related to increased mitotic activity of the interstitial macrophagic population. Ii is suggested that the proliferative burst of these cells may be triggered by the arrival of free particles in the interstitium.
D000818:Animals; D002244:Carbon / Q000378:metabolism*; D002462:Cell Membrane / Q000648:ultrastructure; D002465:Cell Movement; D003593:Cytoplasm / Q000648:ultrastructure; D004848:Epithelium / Q000648:ultrastructure; D008198:Lymph Nodes / Q000648:ultrastructure; D008264:Macrophages / Q000378:metabolism / Q000648:ultrastructure*; D051379:Mice; D009000:Monocytes / Q000648:ultrastructure; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000648:ultrastructure*
D002244:Carbon