Macrophage accumulation, division, maturation, and digestive and microbicidal capacities in tuberculous lesions. I. Studies involving their incorporation of tritiated thymidine and their content of lysosomal enzymes and bacilli.
Dermal and pulmonary tuberculous lesions were produced in rabbits with BCG, biopsied, incubated in vitro with tritiated thymidine ((3)HT) under hyperbaric oxygen, quickly frozen, sectioned in a cryostat, stained for the lysosomal enzyme beta-galactosidase, autoradiographed, stained for acid-fast bacilli and counterstained with hematoxylin. As macrophages developed into epithelioid cells, they could still divide-ie, incorporate (3)HT. However, once they became fully mature epithelioid cells that were 4-plus in beta-galactosidase, they could not do so. Tuberclebacilli did not stimulate macrophage division. On the contrary, macrophages containing bacilli did not divide, except when the lesions began. During the development of tuberculous lesions, macrophages (including those rich in enzymes and those containing bacilli) died, forming caseous centers. Therefore, local cell division did not seem to be the main mechanism by which macrophages reduced their bacillary load. Such division seemed mainly to occur in young macrophages that had recently immigrated into the lesions from the bloodstream and had not yet ingested bacilli.
D000818:Animals; D001345:Autoradiography; D002455:Cell Division; D002478:Cells, Cultured; D005696:Galactosidases / Q000032:analysis; D008264:Macrophages / Q000201:enzymology / Q000276:immunology / Q000378:metabolism; D009163:Mycobacterium bovis; D010587:Phagocytosis; D011650:Pulmonary Alveoli; D011817:Rabbits; D013936:Thymidine / Q000378:metabolism; D014316:Tritium; D014382:Tuberculosis, Cutaneous / Q000201:enzymology / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D014397:Tuberculosis, Pulmonary / Q000201:enzymology / Q000276:immunology / Q000378:metabolism / Q000473:pathology*
D014316:Tritium; D005696:Galactosidases; D013936:Thymidine