Kits
| Article number: | K 6631 |
| Method: | ELISA |
| Tests: | 96 Tests |
| Matrix: | Serum,Plasma |
| Volume: | 100 µl |
| Incubation time: | 1h; 1h; 15 min |
| Standards: | 3.13-25 ng/ml |
| MPO is part of the defence mechanism of the polymorphonuclear leukocytes against exogenic substances. During bacterial infection, these leukocytes, stimulated by chemotactically effective substances (leukotrienes, complement factors, bacterial toxins etc.), move to the site of the infection, where they encapsulate the foreign substances. If the foreign body is located in an intracellular vacuole, different substances are used for the intracellular digestion. Amongst these are MPO, cationic proteins, lysozymes, lactoferrins and some acidic hydrolases. A strong surge of oxidative metabolism takes place, producing a high number of oxygen radicals which leads to the destruction of foreign proteins. Apart of these defence compounds leak into the extracellular space during this process. This happens to a greater extent, when the leukocytes cannot encapsulate the foreign body because of its size or in cases where the neutrophils are destroyed by themselves (through bacterial toxins, crystalline substances etc.). MPO, together with H2O2 and a halogen, forms a very strong anti microbial system, which can effectively combat a number of microorganisms. Apart from its implications in host defense, involvment of MPO has been described in numerous non-infectious diseases such as atherosclerosis, lung cancer, Alzheimer´s disease, and multiple sclerosis. MPO is present and active within atherosclerotic lesions. Numerous lines of evidence suggest mechanistic links between myeloperoxidase, inflammation and both acute and chronic manifestations of cardiovascular disease. Of note, measurements of myeloperoxidase mass and activity may be useful in cardiac risk stratification, both for chronic disease assessment, as well as in identification of patients at risk in the acute setting. Brennan et al. (2003) showed that in 604 sequentially ascertained patients presenting with chest pain, a single initial measurement of plasma myeloperoxidase was an independent early predictor of myocardial infarction, as well as the risk of major adverse cardiac events in ensuing 30-day and 6-month periods. In contrast to troponin T, creatine kinase MB isoform, and C-reactive protein levels, MPO levels identified patients at risk for cardiac events in the absence of myocardial necrosis. SUMMARY: The inflammatory protein myeloperoxidase is present, active and mechanistically poised to participate in the initiation and progression of cardiovascular disease. The many links between myeloperoxidase, oxidation and cardiovascular disease suggest this leukocyte protein may have clinical utility in risk stratification for cardiovascular disease status and outcomes. |