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Dual oxidases represent novel hydrogen peroxide sources supporting mucosal surface host defense
Author(s) -
Geiszt Miklós,
Witta Jassir,
Baff Judit,
Lekstrom Kristen,
Leto Thomas L.
Publication year - 2003
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.02-1104fje
Subject(s) - nadph oxidase , lactoperoxidase , hydrogen peroxide , saliva , reactive oxygen species , microbiology and biotechnology , oxidase test , innate immune system , antimicrobial , phagocyte , mucin , chemistry , enzyme , mucus , thyroid , biology , biochemistry , immune system , immunology , peroxidase , phagocytosis , endocrinology , ecology
Lactoperoxidase (LPO) is an enzyme with antimicrobial properties present in saliva, milk, tears, and airway secretions. Although the formation of microbicidal oxidants by LPO has been recognized for some time, the source of hydrogen peroxide (H 2 O 2 ) for LPO‐catalyzed reactions remains unknown. Reactive oxygen species produced by the phagocyte NADPH oxidase (phox) play a critical role in host defense against pathogens; however, analogous oxidant‐generating systems in other tissues have not been associated with antimicrobial activity. Several homologues of gp91 phox , the catalytic core of this enzyme, were described recently; dual oxidase (Duox)1/thyroid oxidase 1 and Duox2/thyroid oxidase 2 were identified in the thyroid gland and characterized as H 2 O 2 donors for thyroxin biosynthesis. We examined Duox1 and Duox2 expression in secretory glands and on mucosal surfaces and give evidence for their presence and activity in salivary glands, rectum, trachea, and bronchium. Epithelial cells in salivary excretory ducts and rectal glands express Duox2, whereas tracheal and bronchial epithelial cells express Duox1. Furthermore, we detected Duox1‐dependent H 2 O 2 release by cultured human bronchial epithelial cells. Our observations suggest that Duox1 and Duox2 are novel H 2 O 2 sources that can support LPO‐mediated antimicrobial defense mechanisms on mucosal surfaces.