Th1/Th2/Th17/Treg細胞在Ｋ他命膀胱炎患者體內的相互作用
蒙恩1、范綱毅2、程君弘3、張淑貞3、查岱龍1、于大雄1、孫光煥1、吳勝堂1
1國防醫學院 三軍總醫院 外科部 泌尿外科1
2國防醫學院 醫學科學研究所
3國防醫學院 生物及解剖學系
Interplay Among Th1/Th2/Th17/Treg Cells In Ketamine Cystitis Patients
En Meng 1 , Kang-Yi Fang2, Juin-Hong Cherng2,3, Shu-Jen Chang2,3, Tai-Lung Cha1, Guang-Huan Sun1, Dah-Shyong Yu1, Sheng-Tang Wu1
1Division of Urology, Department of Surgery1, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
2Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan
3Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan
Purpose: Chronic ketamine use may cause ulcerative cystitis and bladder dysfunction, commonly referred to ketamine cystitis (KC). The pathogenesis of KC has recently been linked to an immune response to ketamine but has not yet been definitively established. This study proposes a novel immune mechanism to explain the irreversible bladder damage caused by KC.
Materials and Methods: Chronic ketamine use may cause ulcerative cystitis and bladder dysfunction, commonly referred to ketamine cystitis (KC). The pathogenesis of KC has recently been linked to an immune response to ketamine but has not yet been definitively established. This study proposes a novel immune mechanism to explain the irreversible bladder damage caused by KC.
Results: Serum IgE was significantly higher in KC patients (261.59 ± 56.03 IU/ml). KC patients were found to have significantly higher levels of IL-6 (p < 0.05) and IFN-γ (p < 0.001), and significant reduction of TGF-b levels, but comparable levels of IL-2 and IL-4 compared to control patients. KC patients also had significantly higher counts of TH1, TH2, and TH17 cells than healthy volunteers (p = 0.0001).
Conclusion: The immune response of KC may begin with the differentiation of TH17 and continue by alternating between high expression of TH1 and TH2. Suppression of TREG cells may aggravate chronic inflammation in KC patients. The imbalance of TH1, TH2, TH17 and TREG may involve the pathogenesis of KC.