"周邊血液單核球之微小核醣核酸-155,血漿B型肝炎病毒量,和肝臟發炎指標之關係"

Abstract

背景及目標：B型肝炎病毒(HBV)帶原者其體內病毒量的差異非常大。先前的體外實驗研究顯示miR-155可以抑制B型肝炎病毒複製和增強發炎反應。本研究使用已有明確病人特徵的慢性B型肝炎帶原者追蹤世代，目標在於釐清個體之間B型肝炎病毒量之差異和丙氨酸轉胺酶(ALT)的表現量是否受到周邊血液單核球(PBMC)之miR-155表現不同的影響。 材料與方法 :經多時點測量為低病毒量的21位對照，以1:1比例配對經多時點測量為高病毒量的21位個案，我們使用反轉錄聚合酶連鎖反應和即時定量聚合酶連鎖增幅反應分析miR-155於PBMC的表現。 結果 : MiR-155表現量(miR-155ΔCt)和年齡有顯著相關(r=-0.583,p <.0001)。經年齡校正後，miR-155的表現和ALT呈邊緣性統計顯著相關(r=-0.283, p=0.069)。以regulatory T cell 4%為切點進行分層分析，在regulatory T cell>4%的情況下，高病毒量族群的miR-155表現顯著高於低病毒量族群(p=0.0127)，然而，於Treg≦4%的情況之下卻無任何顯著相關。 結論 :年齡校正後，miR-155表現和ALT呈現正相關。Regulatory T cell會修飾miR-155的表現和病毒量之間的關係。

Background : There is a wide range of viral load among hepatitis B virus (HBV) carriers. Preliminary in vitro study suggest that miR-155 may have the capability to inhibit HBV replication and enhancing the inflammation. Using data from a well-characterized cohort of HBV carriers, this study aimed to investigate whether inter-individual differences in HBV viral load and subsequent ALT levels might be influenced by different peripheral blood mononuclear cell (PBMC) expression levels of miR-155. Materials and Methods: 21 controls with repeated measures of low viral load were one-by-one matched to 21 cases with repeated measures of high viral load. We used reverse transcription polymerase chain reaction and real-time quantitative polymerase chain reaction to analyze PBMC mir-155 expression. Results: MiR-155 expression levels (miR-155ΔCt) was correlated with age (r=-0.583, p < .0001). After adjusting for age, the correlation between miR-155 expression and ALT levels approached statistically significant level (r=-0.283, p=0.069). Using regulatory T cell (Treg) 4% as a cutpoint for stratification analysis, miR-155 expression was significantly higher in high viral load group than in low viral load group when Treg was greater than 4% (p=0.0127), whereas no such relationship was found when Treg was≦4% . Conclusion: After adjusting for age, miR-155 expression may be positively associated with ALT. Proportion of Treg may modulate the relationship between miR-155 expression and longitudinal levels of viral load.