Effect of in vitro and in vivo administration of dexamethasone on rat macrophage functions: comparison between alveolar and peritoneal macrophages

Resident alveolar macrophages (AMs) and peritoneal macrophages (PMs), though they originate from common precursor cells, differ morphologically and functionally. The two types of macrophages residing in different tissues may respond differently to glucocorticoids. In the present study, we compared the effects of a synthetic glucocorticoid, dexamethasone (Dex), on rat AMs and PMs with regard to their phagocytic activity and tumour necrosis factor-alpha (TNF-alpha) releasability. In vitro exposure of the macrophages to Dex caused the depression of phagocytic activity of AMs but not of PMs. In contrast, TNF-alpha releasability was depressed in the both types of macrophages, and no difference was found between AMs and PMs in their susceptibility to TNF-alpha regulation by Dex. When Dex was administered subcutaneously into rats, phagocytic activity was severely depressed in AMs but not in PMs. On the other hand, TNF-alpha releasability was depressed both in AMs and PMs by the in vivo Dex administration. The depression in PMs, however, was transitory and less severe than that in AMs. These results suggest that alveolar macrophages and peritoneal macrophages differ intrinsically in responses to glucocorticoid, and that the cell location and the cell's microenvironment can also modulate the effects of glucocorticoid on macrophage functions.

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