慢性部分阻塞性膀胱相關性之免疫反應
林威宇1,2,3,、林依蓓1、黃麗穎1、Robert M. Levin4、陳妙齡5
1嘉義長庚紀念醫院 外科部 泌尿科;2嘉義長庚科技大學;3長庚大學;4Stratton VA Medical Center;5長榮大學 健康科學院 保健營養學系
The Relevance of Immune Responses on Partial Bladder Outlet Obstruction and Reversal
 Wei-Yu Lin1,2,3, Yi-Pai Lin1 , Li-Ying Huang1 , Robert M. Levin4 , and Miaw-Ling Chen5  
Division of Urology, Department of Surgery, Chang Gung Memorial Hospital, Chia-Yi, Taiwan1, Chang Gung University of Science and Technology, Chia-Yi, Taiwan2, Chang Gung University, Taoyuan, Taiwan3, Stratton VA Medical Center, Albany, NY, USA4, Department of Nutrition and Health Sciences, College of Health Science, Innovate Research Center of Medicine, Chang Jung Christian University, Tainan, Taiwan5
 
Purpose: Partial bladder outlet obstruction (PBOO) causes tissue inflammation, significantly increased systemic oxidative stress markers, and the proliferation of circulating myeloid-derived suppressor cells. Since these systemic immunologic responses are associated with PBOO, this study investigated the regulatory mechanism of inflammation and helper T cells.
Materials and Methods: Surgical PBOO was performed in four groups of rats, including control (C), obstruction at 2 (O2) and 4 (O4) weeks, and at 4 weeks after relief of PBOO (R4) (n=6 each). Levels of urinary prostaglandin metabolite (PGEM), expressions of inflammatory cytokines (IL-6 and IL-17) in the bladder, and levels of peripheral blood regulatory T cells (Treg cells) and TGF-β1 were assessed by immuno-histochemistry, flow cytometry, or ELISA.
Results: Levels of urinary PGEM, bladder IL-17, and peripheral Treg cell (Foxp3) and TGF-β1 all significantly increased at 2 and 4 weeks after PBOO. PGEM, IL-17, and Treg cells (Foxp3) were down-regulated after relief of PBOO, while TGF-β1 level further increased.
Conclusion: Transient PBOO triggers an acute, reversible increase in inflammatory cytokines and Treg. The distinct dynamics of individual inflammatory markers suggest that they may be potential parameters for monitoring bladder inflammation.
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    2015-06-04 14:42:00
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