Loss of NLRP3 increases bacterial cystitis via IRAKM.
Transl Androl Urol
; 11(2): 268-276, 2022 Feb.
Article
em En
| MEDLINE
| ID: mdl-35280657
ABSTRACT
Background:
We attempted to characterize the molecular mechanisms that underpin urinary tract infections using a mouse model of cystitis induced by bacterial infection in a background of NOD-, LRR- and PYD domains-containing protein (NLRP3) deficiency.Methods:
Male NLRP3 knockout (NLRP3-/-) and control mice (12 weeks old) were intraurethrally inoculated with 2×108 Escherichia coli (E. coli) and euthanized 1, 3, and 7 days later to assess the degree of bladder infection. Immunohistochemical detection of NLRP3 and interleukin-1 receptor-associated kinase M (IRAKM) was performed. Quantitative PCR analysis was performed to analyze the expression of interleukin (IL)-1ß and tumor necrosis factor (TNF)-α.Results:
Bladder infection was observed in control mice 1 day after inoculation with E. coli. The infection had disappeared by day 7. IL-1ß and TNF-α levels were lower 1 day after injection but higher on days 3 and 7 in the NLRP3-/- group compared with the control mice (P<0.05). Expression of NLRP3 and IRAKM in wild-type (WT) group were significantly decreased 1 day post infection, and by day 7 were increased back to similar level on day 0. On the contrary, in the NLRP3-/- group, IRAKM was significantly lower than WT mice on day 0 and were significantly decreased by day 7.Conclusions:
Deficiency of NLRP3 expression in NLRP3-/- mice contributes to the pathogenesis of chronic inflammation associated with cystitis through IRAKM.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Tipo de estudo:
Prognostic_studies
Idioma:
En
Revista:
Transl Androl Urol
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
China