The relevance of immune responses to partial bladder outlet obstruction and reversal.

Abstract

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. 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. 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. 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.