Flavin Reductase Contributes to Pneumococcal Virulence by Protecting from Oxidative Stress and Mediating Adhesion and Elicits Protection Against Pneumococcal Challenge.

摘要: Pneumococcal flavin reductase (FlaR) is known to be cell-wall associated and possess age dependent antigenicity in children. This study aimed at characterizing FlaR elucidating its involvement pneumococcal physiology virulence. Bioinformatic analysis of sequence identified three-conserved cysteine residues, suggesting a transition metal-binding capacity. Recombinant (rFlaR) bound Fe2+ exhibited FAD-dependent NADP-reductase activity, which increased the presence or excess inhibited by divalent-chelating agents. flaR mutant was highly susceptible H2O2 compared wild type (WT) complemented strains, role for oxidative stress resistance. Additionally, demonstrated significantly decreased mice mortality following intraperitoneal infection. Interestingly, lack did not affect extent phagocytosis primary mouse peritoneal macrophages but reduced adhesion A549 cells WT strains. Noteworthy are findings that immunization with rFlaR elicited protection against lethal challenge anti-FlaR antisera neutralized bacterial Taken together, FlaR's roles virulence, combined significant homology human proteins, point towards as vaccine candidate.