Inhibitory effect of dexamethasone on myeloid differentiation factor 88 and tumor necrosis factor-alpha expressions in mouse peritoneal macrophages.
- Author:
Wen-jie ZHAO
1
;
Li-yan XI
;
Li MA
;
Jun-min ZHANG
;
Xi-qing LI
;
Chang-ming LU
;
Fei LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cells, Cultured; Dexamethasone; pharmacology; Macrophages, Peritoneal; cytology; metabolism; Male; Mice; Mice, Inbred BALB C; Myeloid Differentiation Factor 88; drug effects; genetics; metabolism; Penicillium; growth & development; Tumor Necrosis Factor-alpha; drug effects; genetics; metabolism
- From: Journal of Southern Medical University 2009;29(12):2404-2409
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the inhibitory effect of dexamethasone (DEX) on myeloid differentiation factor 88 (MyD88) and tumor necrosis factor-alpha (TNF-alpha) expression in mouse peritoneal macrophages in innate immune response to Penicillium marneffei (PM).
METHODSMouse peritoneal macrophages were cultured in the presence of heat-inactivated yeast-phase PM with or without DEX, and the protein and mRNA expressions of MyD88 in the macrophages were detected using Western blotting and real-time PCR, respectively. TNF-alpha in the cell culture supernatant was measured with enzyme-linked immunosorbent assay.
RESULTSDEX suppressed TNF-alpha production by the macrophages co-cultured with PM. The expressions of MyD88 were up-regulated by PM stimulation, whose effect was inhibited by the application of DEX.
CONCLUSIONThe inhibitory effect of DEX on PM-induced proinflammatory responses of the macrophage is directly associated with the inhibition of MyD88 expression.
