Myeloperoxidase (MPO) is an enzyme found within the body’s immune cells that serves as a direct indicator of inflammatory activity. Its presence in the blood or tissues signals that the body’s defense system has been activated in response to a perceived threat. MPO’s role is to help eliminate foreign invaders, but elevated levels suggest an underlying biological process, whether acute or chronic, requires investigation. The enzyme’s elevation is a measurable sign of excessive immune cell engagement, not a cause in itself.
Understanding Myeloperoxidase and Its Role
Myeloperoxidase is a heme-containing protein produced primarily by neutrophils, which are the most abundant type of white blood cell. It is stored within specialized compartments of these cells called azurophilic granules, ready for immediate deployment. MPO is a component of the innate immune system, acting as a potent tool to destroy invading pathogens.
The enzyme’s main function is to catalyze a reaction that produces hypochlorous acid (HOCl) from hydrogen peroxide and chloride ions. This powerful oxidant is rapidly deployed by the neutrophil to kill bacteria and other microorganisms during a process known as the respiratory burst. While the release of MPO into the extracellular space is tightly regulated, high circulating levels indicate that large numbers of neutrophils have been activated and have released their contents.
Acute Inflammatory Responses
A rapid and significant spike in MPO levels often correlates with an acute inflammatory event where the immune system is immediately mobilized. Systemic bacterial infections, such as sepsis, trigger a massive and rapid recruitment of neutrophils, leading to a high-volume release of MPO as these cells fight the infection. The goal in this scenario is a swift and overwhelming assault to neutralize the threat.
Immediate tissue injury, such as severe trauma or major surgery, also prompts a localized and systemic acute inflammatory response. Damaged tissue releases signals that attract neutrophils, and their subsequent activation releases MPO to clear debris and prevent microbial colonization. Similarly, an immediate allergic reaction can cause a temporary MPO spike as the immune response mobilizes neutrophils to the site of inflammation. This acute elevation is typically transient, resolving as the body manages the initial threat or injury.
Chronic Inflammatory Diseases
High MPO levels become a concern when the elevation persists over a long period, indicating chronic, low-grade inflammation linked to specific diseases. In cardiovascular disease, MPO plays a direct role in promoting atherosclerosis, the hardening of the arteries. The enzyme is found within atherosclerotic plaques, where it modifies low-density lipoprotein (LDL) cholesterol. This modification makes LDL more easily taken up by macrophages to form foam cells, which are foundational to plaque growth.
MPO also contributes to plaque instability, a significant factor in heart attacks, by degrading the collagen cap that stabilizes the plaque. In metabolic syndrome, including obesity and Type 2 diabetes, MPO levels are often elevated due to persistent, low-level inflammation originating from adipose tissue. The excessive adipose tissue attracts neutrophils and macrophages, and their chronic activation leads to MPO release associated with insulin resistance and increased cardiovascular risk.
Chronic autoimmune disorders, such as Rheumatoid Arthritis (RA) and Inflammatory Bowel Disease (IBD), also show a clear link to elevated MPO. In RA, the enzyme is highly concentrated within the synovial fluid of inflamed joints, where it drives oxidative stress and contributes to the destruction of joint tissue. For IBD, which includes Crohn’s disease and ulcerative colitis, high levels of MPO are detected in the plasma and feces of patients, demonstrating the extensive neutrophil-driven inflammation and tissue damage in the gastrointestinal tract.
Lifestyle and Environmental Contributors
External factors that induce systemic oxidative stress can also trigger MPO release, independent of major infection or diagnosed chronic disease. Active smoking is a well-established contributor, with the chemicals in tobacco smoke causing continuous inflammation in the lungs and vasculature. This chronic exposure leads to persistent neutrophil activation and a measurable increase in circulating MPO levels.
Exposure to environmental air pollution, particularly fine particulate matter (PM), also drives MPO elevation through a similar mechanism. Inhaled pollutants cause respiratory inflammation, which then initiates a systemic inflammatory cascade that activates neutrophils and monocytes, leading to MPO release.
Poor dietary habits, specifically a diet high in saturated fats and processed foods, are another powerful stimulus for MPO elevation. High-fat intake can promote neutrophil infiltration into adipose tissue, enhancing MPO activity and contributing to the low-grade inflammation associated with obesity and metabolic dysfunction.
Implications of High MPO Levels
While MPO is an essential part of the body’s defense, chronically high levels are destructive because the powerful oxidants it produces damage healthy host tissue. The hypochlorous acid generated by MPO contributes to widespread oxidative damage, particularly to proteins and lipids within the blood vessel walls. This sustained damage impairs the function of the endothelium, which is a primary step in the development of vascular disease.
The destructive MPO-generated oxidants also modify high-density lipoprotein (HDL) cholesterol, reducing its ability to protect against atherosclerosis. As a result, MPO is increasingly recognized as a biomarker for risk assessment, particularly in cardiovascular health. Measuring MPO levels provides insight into a patient’s inflammatory and oxidative stress burden, which may predict future risk of major adverse cardiac events, even in individuals with otherwise normal cholesterol levels.