Abstract
Macrophages separated from the granulomatous lungs of tuberculous mice had a high level of cholesterol esters. Resident peritoneal macrophages of normal mice were very low in ester content. When the cells were incubated with mycobacteria in Hanks'' solution, the ester content of the mixture increased greatly. Peritoneal macrophages harvested by induction with casein had many more cholesterol esters than unstimulated resident cells. When such stimulated macrophages were incubated alone in Hanks'' solution, the ester content decreased, probably due to hydrolysis into free form. This reduction was markedly inhibited by incubation with mycobacteria. These observations at a macrophage level presented a cytological explanation for increased cholesterol ester content in mouse lungs with developing granulomatous lesions.

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