The relevance of immune responses to partial bladder outlet obstruction and reversal. Issue 5 (29th October 2016)

• Record Type: Journal Article
• Authors: Lin, Wei‐Yu; Lin, Yi‐Pai; Levin, Robert M.; Chen, Miaw‐Ling
• Is Part Of: Neurourology and urodynamics. Volume 36:Issue 5(2017:Jun.)
• Page Start: 1306
• Page End: 1312
• Publication Date: 2016-10-29
• Subjects: inflammatory cytokine -- partial bladder outlet obstruction -- prostaglandin metabolite -- regulatory T cells; Urinary organs -- Periodicals; Urodynamics -- Periodicals; Urology -- Periodicals; 616.6
• DOI: 10.1002/nau.23136
• Languages: English
• ISSNs: 0733-2467

Abstract

Abstract : Aims: Partial bladder outlet obstruction (PBOO) causes tissue inflammation, a significant increase in markers of systemic oxidative stress, and proliferation of circulating myeloid‐derived suppressor cells. Here, we investigated the regulatory mechanisms underlying inflammation and helper T cell involvement in PBOO. Methods: Surgical PBOO was performed in four groups of rats: control (C), obstruction at 2 (O2) and 4 (O4) weeks, and 4 weeks after the relief of PBOO (R4) ( n = 6 each). The urinary levels of prostaglandin E metabolite (PGEM), expression of inflammatory cytokines (IL‐6 and IL‐17) in the bladder, numbers of peripheral blood regulatory T cells (Treg cells), and levels of TGF‐β1 were assessed via immunohistochemistry, flow cytometry, or ELISA. Results: The levels of urinary PGEM, bladder IL‐17, and TGF‐β1 and the numbers of peripheral Treg cells (Foxp3) were all significantly increased at 2 and 4 weeks after PBOO. PGEM, IL‐17, and Treg cells (Foxp3) were decreased after the relief of PBOO, while the levels of TGF‐β1 continued to increase. Conclusions: Transient PBOO triggers an acute, reversible increase in inflammatory cytokines and Treg cells. The distinct dynamics of individual inflammatory markers support their potential use as markers for monitoring bladder inflammation.