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KMID : 0357119920140010041
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Korean Journal of Immunology
1992 Volume.14 No. 1 p.41 ~ p.52
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Regulation of Tumor Necrosis Factor-alpha Gene Expression by Glucocorticoid, Dehydroepiandrosterone and 1, 25-dihyroxyvitamin D2
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이현철
이준행/신부안/김중렬/강인철/오종석
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Abstract
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The modulating effects of corticosfterone 9GCS), dehydroepiandrosterone (DHEA), and 1, 25-dihyroxyvitamin D3(VD3) on the in vitro production of tumor necrosis factor alpha (TNFα) by lipopolysaccharide (LPS0-stimulated murine macrophages were
investigated. GCS, at concentrations ranging from 10E-9 to 10E-6 M, reduced the TNF production in a dose-dependent manner. In contrast, DHEA ranging from 10E-9 to 10E-6m enhanced TNF production. The decreased production of TNF-α by GCS was not
restored
by DHEA OR VD3 pretreatment but by RU486.
The effects of GCS, DHEA, and VD3 on the regulation of TNF-α gene in human myelomonocytic cell lines (HL-60 and u937 cells) and murine monocyte-macrophage cell line P388D1 were also examined. Phorbol 12-myristate 13-acetate (PMA) strongly induce
the
transcription TNF-α gene after 1, 3hr incubation, whilst the addition of GCS, DHEA, VD3 to PMA-stimulated cells didn't affect the mRNA production by human myelomonocytic cell lines. LPS induced the transcription of TNF-α gene in murine P388D1
cells
after 3hr incubation nd the addition of GCS to LPS-stimulated cells inhibited the mRNA rpoduction, but DHEA and VD3 didn't affect.
These findings suggest that the different stage of myeloid differentiation or the different level of macrophage activation may be related to TNF-α transcription and translation and also suggest that the synthesis of TNF-αcould be increased and
appeared to be regulated post-transeriptionally by DHEA. In addition, the increased innate resistance of mice to Listeria monocytogens infection by HEA or VD3 could be related to the increased TNF production.
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KEYWORD
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