Resistance of Streptococcus pneumoniae to Hypothiocyanous Acid Generated by Host Peroxidases
Heather L. Shearer, Christopher D. Kaldor, Harry Hua, Anthony J. Kettle, Heather A. Parker, Mark B. Hampton
Abstract
, which was converted to HOCl by myeloperoxidase (MPO) present on NETs. However, there was no loss in bacterial viability because HOCl was scavenged by the NET proteins. We conclude that at sites of infection, bacteria will be protected from HOCl by thiocyanate and extracellular proteins including those associated with NETs. Resistance to HOSCN may give S. pneumoniae a survival advantage over other pathogenic bacteria. Understanding the mechanisms by which S. pneumoniae protects itself from HOSCN may reveal novel strategies for limiting the colonization and pathogenicity of this deadly pathogen.
Topics & Concepts
Streptococcus pneumoniaeHypochlorous acidMicrobiologyMyeloperoxidaseLactoperoxidaseBiologyBacteriaThiocyanateMycoplasma pneumoniaeStreptococcaceaePneumococcal infectionsEnzymePseudomonas aeruginosaPeroxidaseExtracellularPathogenic bacteriaPathogenRespiratory burstPseudomonadaceaeHydrogen peroxideNeutrophil extracellular trapsCoxiella burnetiiKlebsiella pneumoniaeAntibody opsonizationRespiratory infectionBiochemistryStreptococcus pyogenesChemistryPneumonia and Respiratory InfectionsNeutrophil, Myeloperoxidase and Oxidative MechanismsImmune Response and Inflammation