Data from: Oxidative killing of encapsulated and nonencapsulated Streptococcus pneumoniae by lactoperoxidase-generated hypothiocyanite

Streptococcus pneumoniae (Pneumococcus) infections affect millions of
people worldwide, cause serious mortality and represent a major economic
burden. Despite recent successes due to pneumococcal vaccination and
antibiotic use, Pneumococcus remains a significant medical problem. Airway
epithelial cells, the primary responders to pneumococcal infection,
orchestrate an extracellular antimicrobial system consisting of
lactoperoxidase (LPO), thiocyanate anion and hydrogen peroxide (H2O2). LPO
oxidizes thiocyanate using H2O2 into the final product hypothiocyanite
that has antimicrobial effects against a wide range of microorganisms.
However, hypothiocyanite’s effect on Pneumococcus has never been studied.
Our aim was to determine whether hypothiocyanite can kill S. pneumoniae.
Bactericidal activity was measured in a cell-free in vitro system by
determining the number of surviving pneumococci via colony forming units
on agar plates, while bacteriostatic activity was assessed by measuring
optical density of bacteria in liquid cultures. Our results indicate that
hypothiocyanite generated by LPO exerted robust killing of both
encapsulated and nonencapsulated pneumococcal strains. Killing of S.
pneumoniae by a commercially available hypothiocyanite-generating product
was even more pronounced than that achieved with laboratory reagents.
Catalase, an H2O2 scavenger, inhibited killing of pneumococcal by
hypothiocyanite under all circumstances. Furthermore, the presence of the
bacterial capsule or lytA-dependent autolysis had no effect on
hypothiocyanite-mediated killing of pneumococci. On the contrary, a
pneumococcal mutant deficient in pyruvate oxidase (main bacterial H2O2
source) had enhanced susceptibility to hypothiocyanite compared o its
wild-type strain. Overall, results shown here indicate that numerous
pneumococcal strains are susceptible to LPO-generated hypothiocyanite.