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KMID : 0370220180620010039
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Yakhak Hoeji
2018 Volume.62 No. 1 p.39 ~ p.48
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Effect of Low Dose Corticosterone Pretreatment on the Production of LPS-Induced Inflammatory Mediators in Endotoxin-Preexposed Cells
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Chae Byeong-Suk
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Abstract
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Low dose glucocorticoids (GCs) are known to have proinflammatory effects in the LPS-stimulated innate immune cells. To investigate whether preconditioning of low dose corticosterone enhances or not LPS-induced production of inflammatory mediators and heper T (Th) cytokines in endotoxin tolerant cells (ET), RAW 264.7 cells and EL4 cells were pretreated with low dose corticosterone (Cort: 50 and 100 ng/ml) and low dose LPS (50 ng/ml) in fresh complete medium once a day for 3 days and then cultured in fresh complete medium for 6 hr or 24 hr in the presence or absence of LPS (1~10 μg/ml) or Con A. In the present study, the results demonstrated that Cort pretreatment strongly enhanced LPS-induced production of TNF-α, IL-6, IL-10, PGE2 and NO by RAW 264.7 cells in a dose-dependent manner in control, whereas Cort pretreatment didn’t affect LPS-induced production of TNF-α, IL-10, PGE2 but significantly enhanced LPS-induced production of IL-6 and NO in ET. Cort pretreatment strongly augmented Con A-induced- production of IFN-γ and IL-10 and ratios of IFN-γ/IL-10 by EL4 cells in a dose-dependent manner in control, whereas Cort 50 ng/ml pretreatment remarkably decreased Con A-induced production of IL-10 and ratios of IFN-γ/IL-10 in ET. Cort pretreatment strongly enhanced LPS-induced production of IFN-γ and IL-10 and attenuated ratios of IFN-γ/IL-10 by EL4 cells in control, whereas Cort pretreatment didn’t affect LPS-induced production of IFN-γ and IL-10 and enhanced ratios of IFN-γ/IL-10 in ET. These findings suggest that preconditioning of low dose corticosterone may enhance production of IL-6 and NO with a shift in the Th1/Th2 balance toward Th1 to secondary infection in a state of endotoxin tolerance, which may lead to low grade inflammation.
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KEYWORD
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Endotoxin tolerance, Corticosterone pretreatment, TNF-α, IL-6, IL-10, IFN-γ, PGE2, NO
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