Myeloperoxidase (MPO) is a heme-containing enzyme found primarily in the azurophilic granules of neutrophils, the most abundant type of white blood cell. When these immune cells are activated, they release MPO into the surrounding tissue and bloodstream. Elevated levels in the circulation serve as an indicator of heightened inflammatory activity and oxidative stress, often measured to assess underlying health risks, particularly those related to the cardiovascular system.
Myeloperoxidase Function and Measurement
The primary function of MPO is to provide a potent defense mechanism against invading pathogens. As part of the innate immune response, MPO uses hydrogen peroxide and chloride ions to generate hypochlorous acid (HOCl), a powerful oxidizing agent highly effective at destroying bacteria and other microorganisms. MPO is also found in monocytes, but the largest stores reside within neutrophils.
Measuring MPO levels in the blood, typically via an enzyme-linked immunosorbent assay (ELISA), gauges systemic inflammation. Although not yet standard in routine physicals, MPO is increasingly analyzed as a specific biomarker, often alongside markers like high-sensitivity C-reactive protein (hs-CRP).
Acute Inflammatory Responses
A rapid and temporary elevation of MPO occurs in response to immediate, short-term threats that trigger neutrophil mobilization. Common acute causes include active bacterial or viral infections, where the immune system is actively fighting a pathogen. The surge in MPO reflects the massive deployment and degranulation of neutrophils at the site of infection or injury.
Acute trauma, such as severe injury or recent surgery, also leads to a transient spike in MPO as the body initiates healing. A particularly relevant acute cause is a heart attack (acute coronary syndrome), where MPO is released from neutrophils infiltrating ruptured atherosclerotic plaque. This sudden release is associated with plaque erosion and destabilization, a mechanism leading to the acute event.
Chronic Systemic Stressors and Cardiovascular Risk
The sustained elevation of MPO is a greater concern, signaling chronic, low-grade inflammation driven by systemic stressors. Major contributors include chronic exposure to tobacco smoke, a potent inducer of oxidative stress, and conditions causing metabolic dysfunction, such as uncontrolled diabetes and obesity.
Chronic inflammatory diseases, including rheumatoid arthritis and inflammatory bowel disease, also maintain the immune system in a state of overdrive. High cholesterol (dyslipidemia) is another key driver because MPO accumulates within atherosclerotic plaques.
Chronic MPO activity is directly implicated in the progression of atherosclerosis, the hardening of the arteries. For individuals with existing coronary artery disease, persistently high MPO levels are strongly associated with an increased risk of future adverse cardiovascular events, including heart attack and stroke. MPO serves as a marker of plaque vulnerability, indicating a heightened risk for plaque rupture.
The Damaging Effects of Elevated MPO
When MPO is chronically elevated, its powerful oxidative activity shifts from fighting pathogens to damaging the body’s own tissues. The persistent generation of reactive oxidant species leads to systemic oxidative stress, impairing normal cellular function. This damage is pronounced in the vascular system, contributing to endothelial dysfunction, the earliest stage of arterial disease.
MPO directly attacks nitric oxide (NO), a molecule that helps blood vessels relax and widen, reducing its bioavailability. This consumption of NO impairs the ability of blood vessels to regulate flow, contributing to hypertension and further vascular damage. MPO also modifies circulating lipoproteins, converting Low-Density Lipoprotein (LDL) into oxidized LDL (ox-LDL). This modified lipoprotein is highly atherogenic, promoting its uptake by immune cells in the artery wall, which leads to plaque growth. MPO also renders High-Density Lipoprotein (HDL) dysfunctional, stripping it of its protective properties.