Secretory IgA, Salivary Peroxidase, and Catalase‐Mediated Microbicidal Activity during Hydrogen Peroxide Catabolism in Viridans Streptococci: Pathogen Coaggregation
Author(s) -
Yoshinari Uehara,
Kazunaga Agematsu,
Ken Kikuchi,
Shigenobu Matsuzaki,
S Imai,
Masaya Takamoto,
Kazuo Sugane,
Tsuyoshi Sugiura,
Yasuhiko Konishi,
Norio Yoshino,
Shotaro Takeuchi,
Heewon Seo,
Shigeru Kuramoto,
Motoyuki Sugai
Publication year - 2006
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/504439
Subject(s) - microbiology and biotechnology , streptococcus sanguinis , saliva , biology , catalase , staphylococcus aureus , viridans streptococci , candida albicans , pathogen , bacteria , streptococcus gordonii , streptococcus pneumoniae , streptococcus mutans , streptococcaceae , streptococcus , antibiotics , biochemistry , enzyme , genetics
Viridans streptococci can kill methicillin-resistant Staphylococcus aureus (MRSA) through the production of hydrogen peroxide (H2O2). However, several hundred viridans streptococci cells are necessary to kill 1 cfu of MRSA. We analyzed the potency of bactericidal and fungicidal effector molecules induced by catabolism of H2O2 in the oral cavity. Secretory IgA (SIgA) and an unidentified salivary component bound Streptococcus sanguinis, a viridans streprococcus, and MRSA into coaggregates. In these coaggregates, salivary peroxidase and the MRSA catalase produced singlet molecular oxygen (1O2) from H2O2 produced by viridans streptococci. SIgA converted 1O2 into ozone, which has potent bactericidal and fungicidal activity. We calculated that <10 cfu of Streptococcus sanguinis were necessary to kill 1 cfu of MRSA in the coaggregate. SIgA, Aspergillus niger catalase, and H2O2 in saliva killed Candida albicans, which is highly resistant to reagent H2O2. Together with indigenous bacteria and innate immunity, SIgA potentially constitutes a novel system that may sustain oral homeostasis.
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