Endocrine regulation of murine macrophage function: effects of dehydroepiandrosterone, androstenediol, and androstenetriol.
In these studies, the in vitro influences of dehydroepiandrosterone (DHEA), androstenediol (AED), and androstenetriol (AET) on proinflammatory cytokine production from macrophages was examined. From physiologic to pharmacologic doses, DHEA suppressed secretion of each pro-inflammatory cytokine while AED had little influence on the responses. In sharp contrast, AET augmented TNF-alpha and IL-1 secretion while not influencing IL-6 production. Furthermore, the antiglucocorticoid activity of DHEA, AED, and AET was also investigated. Co-culture with AET counteracted the down-regulatory effect of hydrocortisone on LPS-induced TNF-alpha and IL-1 secretion. These data imply that AET is capable of regulating cytokine secretion from macrophages and may function to counterbalance glucocorticoid function.
Padgett
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Department of Oral Biology, College of Dentistry, The Ohio State University, Columbus 43210, USA. padgett.11@osu.edu
Loria
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D045930:Anabolic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D015114:Androstenediol / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002478:Cells, Cultured / Q000187:drug effects; D003687:Dehydroepiandrosterone / Q000008:administration & dosage / Q000494:pharmacology*; D004702:Endocrine Glands / Q000187:drug effects*; D006854:Hydrocortisone / Q000494:pharmacology; D007375:Interleukin-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008262:Macrophage Activation / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D045930:Anabolic Agents; D000893:Anti-Inflammatory Agents; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D003687:Dehydroepiandrosterone; D015114:Androstenediol; D006854:Hydrocortisone