地塞米松对 F．monophora 感染巨噬细胞模式识别受体及炎症因子表达的影响

摘要

目的：探讨F．monophora体外感染模型中地塞米松（ DEX）对模式识别受体及免疫炎症因子表达的影响。方法：实验分为四组：F．monophora与加入 DEX的巨噬细胞共培养组、F．monophora与巨噬细胞共培养组、单纯加入DEX的巨噬细胞组及巨噬细胞空白对照组。定量PCR检测各组中模式识别受体Dectin-1、TLR-2、TLR-4的表达；ELISA法测定培养上清中TNF-α的表达量。结果：F．monophora与巨噬细胞共培养组相对于空白对照组及单纯加入 DEX 组的 Dectin-1表达显著升高，在加入 DEX 后Dectin-1表达明显受到抑制（t ＝121900， P ＜0．05）；加入 DEX 的共培养组中 TLR-2表达增加，但与F．monophora和巨噬细胞共培养组相比，差异无统计学意义（ t＝3022， P＞0.05）；F．monophora感染引起TLR-4显著下调，加入DEX对TLR-4表达无影响（t＝2021，P＞0.05）。相对于F．monophora与巨噬细胞共培养组，DEX共培养组中巨噬细胞分泌TNF-α的量显著下调（t＝1514000， P＜0.05）。结论：DEX可抑制巨噬细胞Dectin-1的表达，并下调 TNF-α的表达量，进而使机体处于免疫耐受状态，但对TLR-2、TLR-4表达无明显影响。%To explore the effects of dexamethasone to the expression of pattern rec-ognition receptors ( PRRs ) and inflammatory cytokine production by macrophage in an in vitro model of infection.Methods:Four groups were established to evaluate the effects of DEX to PRRs, including F.monophora+DEX+macrophage group, F.monophora+macrophage group, DEX+macrophage group and negative control groups.The mRNA expression levels of Dectin-1, TLR-2, TLR-4 were determined by real time PCR.The secretion of TNF-αin culture supernatant was determined by ELISA.The groups including DEX only and normal macrophage were used as control.Results:The expression of Dectin-1 increased significantly in the F.monophora+macro-phage group, but decreased after DEX was added in the F.monophora+DEX group( t=121 900, P<0.05) .The expression of TLR-2 increased in the F.monophora+DEX group, but not signifi-cant statistically(t=3 022, P>0.05).The expression of TLR-4 was down regulated in F.mono-phora+macrophage group, while no difference was detected when DEX was added ( t=2 021, P>0.05).The secretion of TNF-αwas decreased significantly in F.monophora+DEX group in comparison to F.monophora infection group (t=1 514 000, P<0.05).Conclusion:DEX most likely down-regulated the expression of Dectin-1 and the secretion of TNF-α, which resulted in im-mune tolerance in F.monophora infected macrophage in this in vitro model of infection.Yet, no significant effects were observed in expression levels of TLR-2、TLR-4 statistically.