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：研究中藥當歸芍藥散對外周血T淋巴細胞轉錄因子GATA-3和T-bet mRNA表達的影響，初步探討其用于治療不明原因反復自然流產的可能性。方法：體外分離提取11例志愿者外周血單核細胞，在含有或不含當歸芍藥散的培養液中培養24h，用實時定量PCR技術檢測GATA-3和T-bet mRNA的表達。結果：用10 μg/mL濃度當歸芍藥散處理后,單核細胞中GATA-3 mRNA的含量與對照組比較顯著增高（P＜0.05)。當歸芍藥散處理細胞后，T-bet mRNA的表達水平呈降低趨勢，當濃度為100 μg/mL時，與對照組比較有顯著性差異（P＜0.05)。結論：當歸芍藥散可上調轉錄因子GATA-3 mRNA的表達或下調T-bet mRNA的表達,從而可能通過調節Th2/Th1平衡向Th2偏移、對于Th1反應異常增強的不明原因反復自然流產有一定的治療潛能。