Bacteria such as Pseudomonas aeruginosa and fungi such as Candida albicans are killed in this manner.Neutrophils are also involved in killing extracellular pathogens (pathogens outside of the cell) through the release of NETs. These NETs contain myeloperoxidase, among other antimicrobial proteins. Once released outside of the cell, NETs trap pathogens and may in some cases kill them. Although myeloperoxidase is not required for all NET formation/release, NETs are only formed and released in response to Candida albicans when myeloperoxidase is present. Myeloperoxidase proteins in NETs can still react with H2O2 to form HClO and break down some extracellular pathogens. In myeloperoxidase deficient individuals, this extracellular pathogen killing doesn’t typically occur.Finally, during infection, neutrophils can migrate to the lymph nodes, where they deposit myeloperoxidase. Although the mechanisms of this process aren’t well understood, there is evidence that this extracellular myeloperoxidase interacts with dendritic cells (cells of the adaptive immune system) in the lymph nodes, leading to a decrease in adaptive immune system activity in response to infection. Presentation
About 1:1,000 to 1:4,000 individuals in the United States and Europe and 1:55,000 individuals in Japan experience myeloperoxidase deficiency. The most common symptom of myeloperoxidase deficiency is frequent infections, particularly by the fungus Candida albicans. This symptom is especially frequent in individuals who also experience diabetes mellitus.The majority of myeloperoxidase-deficient individuals, however, do not display any significant tendencies towards chronic infections from most bacteria.
Specific stains bind to myeloperoxidase, and individuals who display large, granulated cells without this stain through flow cytometry typically have myeloperoxidase deficiency. In this way, it’s apparent when neutrophils are present in an individual but peroxidase activity is absent.Note, myeloperoxidase deficiency can cause false positives in the diagnosis of chronic granulomatous disease, a condition which includes dysfunctional NADPH oxidase. Both disorders interfere with neutrophils’ abilities to kill pathogens through reaction with oxidative species. However, chronic granulomatous disease leads to inadequate H2O2 production, while myeloperoxidase deficiency is characterized by a lack of myeloperoxidase to interact with present H2O2. Testing with NADPH oxidase-specific assays can lead to positive results for chronic granulomatous disease and negative results for myeloperoxidase deficiency. Treatment
Most individuals with myeloperoxidase deficiency do not need regular treatment, as they experience only mild symptoms, if any at all. Continued antibiotic use is not recommended in myeloperoxidase-deficient patients who don’t experience recurrent infections.Acquired myeloperoxidase deficiency typically goes away when the underlying condition is treated. In particular, when myeloperoxidase deficiency is caused by severe iron deficiency, treatment with iron returns myeloperoxidase function to normal. References


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