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Neutrophil extracellular traps
Recently, scientists in Germany described a novel tool with which neutrophils enhance killing of extracellular pathogens while minimizing damage to the host cells. Upon in-vitro activation with the pharmacological agent phorbol myristate acetate (PMA), IL-8 or LPS, neutrophils release granule proteins and chromatin to form an extracellular fibril matrix, i.e. neutrophil extracellular traps (NETs) through an active process. More recently, it has also been shown that not only bacteria but also pathogenic fungi such as C. albicans induces neutrophils to form NETs that capture and kill C. albicans hyphal as well as yeast-form cells. NETs disarm pathogens with antimicrobial proteins such as neutrophil elastase and histones that are bound to the DNA. NETs provide for a high local concentration of antimicrobial components and bind, disarm, and kill microbes extracellularly independent of phagocytic uptake. In addition to their antimicrobial properties, NETs may serve as a physical barrier that prevents further spread of the pathogens. Furthermore, delivering the granule proteins into NETs may keep potentially injurious proteins like proteases from diffusing away and inducing damage in tissue adjacent to the site of inflammation. NETs might also have a deleterious effect on the host, because the exposure of extracellular histone complexes could play a role during the development of autoimmune diseases like lupus erythematosus. NETs could also play a role in inflammatory diseases, as NETs could be identified in preeclampsia, a pregnancy related inflammatory disorder in which neutrophils are known to be activated. These observations suggest that NETs might play an important role in the pathogenesis of infectious and inflammatory disorders.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Neutrophil_extracellular_traps". A list of authors is available in Wikipedia.|