Kits
Myeloperoxidase (IDK® Myeloperoxidase) [MPO], ELISA
Kits
Description
MPO is part of the defence mechanism of the polymorphonuclear leukocytes against
exogenic substances. During bacterial infection, these leukocytes are stimulated
by chemotactically effective substances (leukotrienes, complement factors, bacterial
toxins etc.). They move to the site of the infection and encapsulate the foreign
substances. If the foreign agent is located in an intracellular vacuole, different substances
are used for the intracellular digestion. Amongst these are MPO, cationic proteins,
lysozyme, lactoferrin 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. Some of these molecules can 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 bacterial toxins, crystalline substances etc.).
MPO, together with hydrogen peroxide and a halogen, forms a very strong anti microbial
system, which can effectively combat a number of microorganisms. MPO is
present at high concentration in neutrophil granulocytes, whereas hydrogen peroxide
is produced during infection/ inflammation. The MPO system is inhibited by catalase,
excess of hydrogen peroxide and other reducing substances (e.g. ascorbic acid,
glutathione). In the absence of these agents other cells in the extracellular space can
be affected (e.g. spermatocyte, erythrocytes, leukocytes, and tumor cells)
Apart from its implications in host defence, involvement 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.
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 may identify
patients at risk for cardiac events in the absence of myocardial necrosis.
exogenic substances. During bacterial infection, these leukocytes are stimulated
by chemotactically effective substances (leukotrienes, complement factors, bacterial
toxins etc.). They move to the site of the infection and encapsulate the foreign
substances. If the foreign agent is located in an intracellular vacuole, different substances
are used for the intracellular digestion. Amongst these are MPO, cationic proteins,
lysozyme, lactoferrin 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. Some of these molecules can 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 bacterial toxins, crystalline substances etc.).
MPO, together with hydrogen peroxide and a halogen, forms a very strong anti microbial
system, which can effectively combat a number of microorganisms. MPO is
present at high concentration in neutrophil granulocytes, whereas hydrogen peroxide
is produced during infection/ inflammation. The MPO system is inhibited by catalase,
excess of hydrogen peroxide and other reducing substances (e.g. ascorbic acid,
glutathione). In the absence of these agents other cells in the extracellular space can
be affected (e.g. spermatocyte, erythrocytes, leukocytes, and tumor cells)
Apart from its implications in host defence, involvement 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.
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 may identify
patients at risk for cardiac events in the absence of myocardial necrosis.