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Updated: Aug 19, 2026

Fast and Specific Assessment of the Halogenating Peroxidase Activity in Leukocyte-enriched Blood Samples
Published on: July 28, 2016
Myeloperoxidase: friend and foe
1Department of Medicine, University of Washington School of Medicine, Seattle, WA 98195-7185, USA. seym@u.washington.edu
Abstract:
Neutrophilic polymorphonuclear leukocytes (neutrophils) are highly specialized for their primary function, the phagocytosis and destruction of microorganisms. When coated with opsonins (generally complement and/or antibody), microorganisms bind to specific receptors on the surface of the phagocyte and invagination of the cell membrane occurs with the incorporation of the microorganism into an intracellular phagosome. There follows a burst of oxygen consumption, and much, if not all, of the extra oxygen consumed is converted to highly reactive oxygen species. In addition, the cytoplasmic granules discharge their contents into the phagosome, and death of the ingested microorganism soon follows. Among the antimicrobial systems formed in the phagosome is one consisting of myeloperoxidase (MPO), released into the phagosome during the degranulation process, hydrogen peroxide (H2O2), formed by the respiratory burst and a halide, particularly chloride. The initial product of the MPO-H2O2-chloride system is hypochlorous acid, and subsequent formation of chlorine, chloramines, hydroxyl radicals, singlet oxygen, and ozone has been proposed. These same toxic agents can be released to the outside of the cell, where they may attack normal tissue and thus contribute to the pathogenesis of disease. This review will consider the potential sources of H2O2 for the MPO-H2O2-halide system; the toxic products of the MPO system; the evidence for MPO involvement in the microbicidal activity of neutrophils; the involvement of MPO-independent antimicrobial systems; and the role of the MPO system in tissue injury. It is concluded that the MPO system plays an important role in the microbicidal activity of phagocytes.
Insights
Neutrophils use the myeloperoxidase (MPO) system, involving hydrogen peroxide (H2O2) and halides, to destroy microbes. This MPO-H2O2-halide system is crucial for phagocyte microbicidal activity and can also cause tissue injury.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Neutrophilic polymorphonuclear leukocytes (neutrophils) are key immune cells specialized for phagocytosing and destroying microorganisms.
- Phagocytosis involves opsonin-coated microbes binding to neutrophil receptors, followed by intracellular incorporation into a phagosome.
- A respiratory burst generates reactive oxygen species, and neutrophil granules release antimicrobial substances into the phagosome.
Purpose of the Study:
- To review the sources of hydrogen peroxide (H2O2) for the myeloperoxidase (MPO) system within phagocytes.
- To examine the toxic products generated by the MPO-H2O2-halide system.
- To assess the role of the MPO system in neutrophil microbicidal activity and its potential contribution to tissue injury.
Main Methods:
- Literature review focusing on the myeloperoxidase (MPO) system in neutrophils.
- Analysis of evidence for MPO-dependent and MPO-independent antimicrobial mechanisms.
- Evaluation of the MPO system's role in both microbial killing and host tissue damage.
Main Results:
- The myeloperoxidase (MPO) system, utilizing hydrogen peroxide (H2O2) and halides, produces potent antimicrobial agents like hypochlorous acid.
- These toxic MPO system products can be released extracellularly, potentially contributing to inflammation and tissue damage.
- Evidence supports the significant involvement of the MPO system in the microbicidal capacity of phagocytes.
Conclusions:
- The myeloperoxidase (MPO) system is a critical component of the neutrophil's antimicrobial arsenal, essential for effective pathogen destruction.
- While vital for host defense, the MPO system's reactive products also pose a risk for collateral tissue injury.
- Understanding the MPO system's dual role is crucial for comprehending inflammatory diseases and developing targeted therapies.
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