Transient increase in circulating myeloid-derived suppressor cells after partial bladder outlet obstruction.
J Urol
; 192(5): 1569-73, 2014 Nov.
Article
em En
| MEDLINE
| ID: mdl-24840536
PURPOSE: Partial bladder outlet obstruction causes a significant increase in tissue and systemic oxidative stress markers and tissue inflammatory cytokine levels. Myeloid-derived suppressor cells, IFN-γ, IL-10 and aldosterone are believed to be associated with oxidative stress and inflammation. We investigated alterations in plasma myeloid-derived suppressor cells, IFN-γ, IL-10 and aldosterone levels in partial bladder outlet obstruction and after its reversal. MATERIALS AND METHODS: Rats with surgically induced partial bladder outlet obstruction were divided into 4 groups of 3 each, including sham treated, 4-week obstruction, and 4 and 8-week obstruction with relief. Plasma levels of circulating myeloid-derived suppressor cells, IFN-γ, IL-10 and aldosterone were assessed by flow cytometry or enzyme-linked immunosorbent assay. RESULTS: The circulating myeloid-derived suppressor cell level was markedly increased in the obstruction group compared to the sham treated group and it returned to normal in the 4 and 8-week obstruction with relief groups. Plasma IFN-γ, IL-10 and aldosterone were similarly increased in the obstruction group and returned to normal in the 4 and 8-week obstruction with relief groups. CONCLUSIONS: Levels of circulating myeloid-derived suppressor cells, IFN-γ, IL-10 and aldosterone were increased in rats with partial bladder outlet obstruction but returned to normal after reversal. This suggests that an increase in these parameters may be a good predictive indicator of patients at increased risk for urinary symptoms.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Bexiga Urinária
/
Obstrução do Colo da Bexiga Urinária
/
Citocinas
/
Estresse Oxidativo
/
Células Mieloides
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
J Urol
Ano de publicação:
2014
Tipo de documento:
Article
País de afiliação:
Taiwan