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Myeloperoxidase
1Department of Medicine, University of Washington, Seattle 98195-7185, USA.
Abstract:
Phagocytes respond to stimulation with a burst of oxygen consumption, and much, if not all, of the extra oxygen consumed in the respiratory burst is converted first to the superoxide anion and then to hydrogen peroxide (H2O2). Myeloperoxidase (MPO), which is released from cytoplasmic granules of neutrophils and monocytes by a degranulation process, reacts with the H2O2 formed by the respiratory burst to form a complex that can oxidize a large variety of substances. Among the latter is chloride, which is oxidized initially to hypochlorous acid, with the subsequent formation of chlorine and chloramines. These products of the MPO-H2O2-chloride system are powerful oxidants that can have profound biological effects. The primary function of neutrophils is the phagocytosis and destruction of microorganisms, and the release of MPO and H2O2 into the phagosome containing the ingested microorganism generally leads to a rapid microbicidal effect. Neutrophils from patients with chronic granulomatous disease (CGD) have a microbicidal defect that is associated with the absence of a respiratory burst and, thus, H2O2 production. Neutrophils from patients with a hereditary MPO deficiency, who lack MPO, also have a microbicidal defect, although it is not as severe as that seen in CGD. MPO and H2O2 also can be released to the outside of the cell where a reaction with chloride can induce damage to adjacent tissue and, thus, contribute to the pathogenesis of disease. It has been suggested that pulmonary injury, renal glomerular damage, and the initiation of atherosclerotic lesions may be caused by the MPO system.
Insights
The myeloperoxidase (MPO) system, using hydrogen peroxide (H2O2), destroys microbes but can also damage host tissues. Defects in MPO or H2O2 production impair microbicidal activity and contribute to disease pathogenesis.
Area of Science:
- Immunology
- Biochemistry
- Cell Biology
Background:
- Phagocytes utilize a respiratory burst, producing superoxide anion and hydrogen peroxide (H2O2), to combat pathogens.
- Myeloperoxidase (MPO), released from neutrophils and monocytes, utilizes H2O2 to generate potent oxidants.
- These oxidants, including hypochlorous acid, are crucial for microbial destruction but can also harm host tissues.
Purpose of the Study:
- To elucidate the role of the myeloperoxidase (MPO)-hydrogen peroxide (H2O2)-chloride system in phagocyte function.
- To investigate the consequences of MPO and H2O2 production on both microbial killing and host tissue damage.
- To understand the implications of MPO deficiency and chronic granulomatous disease (CGD) on immune response and disease.
Main Methods:
- Analysis of phagocyte respiratory burst activity and H2O2 production.
- Assessment of MPO release and its enzymatic activity.
- Evaluation of microbicidal function in neutrophils from healthy individuals and patients with MPO deficiency or CGD.
- Investigation of MPO system's role in potential tissue damage mechanisms.
Main Results:
- The MPO-H2O2-chloride system effectively kills ingested microorganisms within phagocytes.
- Neutrophils lacking MPO or the respiratory burst (seen in CGD) exhibit impaired microbicidal activity.
- Extracellular release of MPO and H2O2 can lead to oxidative damage to adjacent host tissues.
- The MPO system is implicated in the pathogenesis of conditions like pulmonary injury and atherosclerosis.
Conclusions:
- The MPO system is a critical component of the innate immune response for microbial killing.
- Dysregulation of the MPO system, due to deficiency or excessive activity, contributes to both impaired immunity and tissue injury.
- Understanding the dual role of MPO is essential for comprehending host defense and inflammatory diseases.
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