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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.

NLRX1 is not involved in the host defense against Escherichia coli induced pyelonephritis