The role of phagocyte NADPH Oxidase (NOX2) in modulating the antimicrobial and inflammatory functions of mouse neutrophils

Urinary tract infections (UTI) stand as one of the most prevalent infections worldwide. Uropathogenic Escherichia coli (UPEC) is the primary cause of UTI, instigating 75% of uncomplicated and 65% of complicated UTIs. Innate immune cells play pivotal roles in eliminating invading uropathogens and represent a potential therapeutic target for UTI prevention and treatment. Previous studies in our laboratory demonstrated that selective depletion of neutrophils during experimental UTI, results in an uncontrolled infection and augmented bladder and kidney pathologies. However, the exact antimicrobial mechanisms employed by neutrophils to eliminate multi-drug resistant uropathogens, such as UPEC, and resolve UTI remain poorly understood. Our dataset provides insight of the multifaceted role of neutrophil NOX2 in UPEC elimination and regulation of inflammatory and effector functions of these innate immune cells. Our transcriptome analyses revealed a heightened pro-inflammatory profile in NOX2-deficient neutrophils compared to WT neutrophils after UPEC stimulation. To investigated the role of NOX2 in modulating neutrophil functions against uropathogenic E coli (UPEC). We harvested neutrophils from wilde-type (WT) and NOX2 KO (Cybb-/-) mice. Isolated neutrophils were stimulated with UPEC or PBS (vehicle) and total RNA was extracted from these cells to perform gene expression analysis.