Abstract
Background: Urinary tract infections (UTIs) caused by uropathogenic Escherichia coli (E. coli) are one of the most prominent infections that have serious impact on kidney functioning and the development of chronic kidney disease. NOD-like receptor (NLR)X1 is an innate immune receptor that is important for immune metabolism and regulation, with as yet an unknown role in UTI and the pathophysiology of pyelonephritis. Methods: Wild-type (WT) and NLRX1 Knock-out (KO) female mice were subjected to UTI by intravesically inoculation of uropathogenic E. coli and sacrificed at 24h and 48h after infection after which bacterial burden and the inflammatory response in the bladder and kidney were studied. Ex vivo we studied the role of NLRX1 during the LPS induced pro-inflammatory cytokine response and phagocytosis of E. coli by granulocytes and monocytes. Results: Here, we report that during early experimental UTI NLRX1 absence reduces bacterial clearance in the bladder and dampens the inflammatory cytokine response, whereas in the kidney NLRX1 does not affect bacterial burden or cytokine response. In addition, we found that NLRX1 is not essential for the pro-inflammatory cytokine secretion by granulocytes and monocytes in response to LPS nor for bacterial phagocytosis. Conclusion: Together, we report that NLRX1 is important in enhancing the early host defense against uropathogenic E. coli in the bladder but does not affect the development of pyelonephritis.
Highlights
Toll like receptors (TLRs) and NOD-like receptors (NLRs) are members of a large family of extracellular and intracellular pattern recognition receptors (PRRs) that trigger immune responses to prevent pathogen invasion and growth[1,2]
To get more insight in NODlike receptor X1 (NLRX1) functioning during bacterial infection we investigated in the present study the role of NLRX1 during uropathogenic E. coli-induced lower and upper Urinary tract infections (UTIs) in mice
Local NLRX1 expression in the bladder and kidney during experimental UTI To determine whether NLRX1 expression is modulated in the murine bladder and kidney during urinary tract infection (UTI), wild-type (WT) mice were intravesically inoculated with uropathogenic E. coli and sacrificed at 24h and 48h after infection
Summary
Toll like receptors (TLRs) and NOD-like receptors (NLRs) are members of a large family of extracellular and intracellular pattern recognition receptors (PRRs) that trigger immune responses to prevent pathogen invasion and growth[1,2]. UTIs are caused by the presence of uropathogenic bacteria, usually Escherichia coli (E. coli), in the lower urinary tract (bladder) that overcome the host innate immune defense. Urinary tract infections (UTIs) caused by uropathogenic Escherichia coli (E. coli) are one of the most prominent infections that have serious impact on kidney functioning and the development of chronic kidney disease. Methods: Wild-type (WT) and NLRX1 Knock-out (KO) female mice were subjected to UTI by intravesically inoculation of uropathogenic E. coli and sacrificed at 24h and 48h after infection after which bacterial burden and the inflammatory response in the bladder and kidney were studied. Conclusion: Together, we report that NLRX1 is important in enhancing the early host defense against uropathogenic E. coli in the bladder but does not affect the development of pyelonephritis
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