Increased gene expression of TGF‐β in peripheral blood mononuclear cells from renal transplant patients with polyomavirus BK viremia |
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Authors: | Wen‐Yao Yin Ming‐Che Lee Hsien‐Bin Huang Ming‐Chi Lu |
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Affiliation: | 1. Division of General Surgery, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan;2. School of Medicine, Tzu Chi University, Hualien, Taiwan;3. Department of General Surgery, Hualien Tzu Chi Medical Center, Hualien, Taiwan;4. Department of Life Science and Institute of Molecular Biology, National Chung Cheng University, Chiayi, Taiwan;5. Division of Allergy, Immunology and Rheumatology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan |
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Abstract: | We aimed to investigate the roles of cytokines during polyomavirus BK (BKV) reactivation in renal transplant patients. Forty‐eight renal allograft recipients were enrolled, and their sera BKV viral load and mRNA expression levels of cytokines in peripheral blood mononuclear cells were measured by real‐time polymerase chain reaction. Patient's age and gene expression levels of interleukin (IL)‐2 (10.04 ± 2.63 vs. 8.70 ± 2.40, p = 0.049) and transforming growth factor (TGF)‐β (12.58 ± 2.59 vs. 10.89 ± 1.91, p = 0.015) were significantly higher in BKV viremia (+) renal transplant patients. Multivariate logistic regression analysis revealed that age and mRNA expression levels of TGF‐β, but not IL‐2, significantly correlated with the presence of BKV viremia. Sera BKV viral loads showed a positive correlation with patient age and the levels of TGF‐β and IL‐6 mRNA. After adjusting for age and sex in the regression model, both age and TGF‐β mRNA levels maintained a significant positive association with sera BKV viral loads. Serum TGF‐β concentration tended to be higher in BKV viremia (+) patients (p = 0.079). In conclusion, expression levels of TGF‐β were found to correlate with both BKV viremia positivity and sera BKV viral loads in renal transplant patients. |
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Keywords: |
BKV
cytokines IL‐2 IL‐6 renal transplant TGF‐β |
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