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Updated: Mar 12, 2026
Nerve-sparing Mid-urethral Obstruction NeMO in Female Small Rodents
Published on: April 25, 2017
The relevance of immune responses to partial bladder outlet obstruction and reversal
Wei-Yu Lin1,2,3, Yi-Pai Lin1, Robert M Levin4
1Division of Urology, Department of Surgery, Chang Gung Memorial Hospital, Chiayi, Taiwan.
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.
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