Objective To investigate the modulating roles of Clara cell secretory 16 kD protein ( CC-16) , transcription factor T-bet, and GATA-3 in airway inflammation of patients with asthma. Methods 25 patients with acute exacerbation of asthma were enrolled as an asthma group and 33 healthy volunteers were enrolled as control. The plasma levels of CC16, IFN-γ, and IL-4 were measured by enzyme-linked immunosorbent assay ( ELISA) . The mRNA expressions of T-bet and GATA-3 in the peripheral bloodmononuclear cells ( PBMCs) were measured by reverse transcription-polymerase chain reaction ( RT-PCR) .Results The levels of CC16 and IFN-γin the asthma group were lower than those in the control group [ ( 21. 96 ±7. 31 ) ng/mL vs. ( 64. 88 ±25. 27) ng/mL, ( 118. 73 ±22. 59) pg/mL vs. ( 145. 53 ±29. 50) pg/mL, both P lt;0. 01] . The IL-4 level in the asthma group was significantly higher than that in the control group [ ( 425. 22 ±4. 37) pg/mL vs. ( 69. 72 ±10. 15 ) pg/mL, P lt; 0. 01] . The T-bet mRNA expression and T-bet /GATA-3 ratio of PBMCs in the asthma group were significantly lower than those in the control group( both P lt; 0. 01) . The expression GATA-3 mRNA was significantly higher than that in the control group( P lt;0. 01) . The level of CC16 was positively correlated with T-bet mRNA expression and the ratio of T-bet /GATA-3 ( r =0. 792, 0. 761, respectively, P lt; 0. 01) . There was no correlation between CC16 and the GATA-3 mRNA expression ( P gt;0. 05) . Conclusions These results suggest that CC16 and T-bet play important protection roles in the pathogenesis of asthma. GATA-3, IFN-γ, and IL-4 also participate in the airway inflammation of asthma.
目的：研究中药当归芍药散对外周血T淋巴细胞转录因子GATA-3和T-bet mRNA表达的影响，初步探讨其用于治疗不明原因反复自然流产的可能性。方法：体外分离提取11例志愿者外周血单核细胞，在含有或不含当归芍药散的培养液中培养24h，用实时定量PCR技术检测GATA-3和T-bet mRNA的表达。结果：用10 μg/mL浓度当归芍药散处理后,单核细胞中GATA-3 mRNA的含量与对照组比较显著增高（P＜0.05)。当归芍药散处理细胞后，T-bet mRNA的表达水平呈降低趋势，当浓度为100 μg/mL时，与对照组比较有显著性差异（P＜0.05)。结论：当归芍药散可上调转录因子GATA-3 mRNA的表达或下调T-bet mRNA的表达,从而可能通过调节Th2/Th1平衡向Th2偏移、对于Th1反应异常增强的不明原因反复自然流产有一定的治疗潜能。