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Kuitenkin artikkelissa huomataan että kyse on eosinofileista ja mastsoluista
reaktioaineitten muodostuksessa, joten mastsolustabilaattoreita
on esim Lomudal, Na- kromoglikat lääke. ja LTE4- sarjan reaktiota taas lieventää montelukast, antileukotrieenilääke, Singulair.
https://en.wikipedia.org/wiki/Eoxin
- charlotte Edenius *,
- Lennart Lindbom ‡ ,
- Magnus Björkholm ‖ , and
- Hans-Erik Claesson * , † , **
-
Communicated by Bengt Samuelsson, Karolinska Institutet, Stockholm, Sweden, November 2, 2007 (received for review July 27, 2007)
Abstract
Human eosinophils contain
abundant amounts of 15-lipoxygenase (LO)-1. The biological role of
15-LO-1 in humans, however, is
unclear. Incubation of eosinophils with
arachidonic acid led to formation of a product with a UV absorbance
maximum at 282
nm and shorter retention time than
leukotriene (LT)C4 in reverse-phase HPLC. Analysis with positive-ion electrospray tandem MS identified this eosinophil metabolite as 14,15-LTC4. This metabolite could be metabolized to 14,15-LTD4 and 14,15-LTE4 in eosinophils. Because eosinophils are such an abundant source of these metabolites and to avoid confusion with 5-LO-derived
LTs, we suggest the names eoxin (EX)C4, -D4, and -E4 instead of 14,15-LTC4, -D4, and -E4, respectively.
Cord blood-derived mast cells and surgically removed nasal polyps from allergic subjects also produced EXC4. Incubation of eosinophils with arachidonic acid favored the production of EXC4, whereas challenge with calcium ionophore led to exclusive formation of LTC4.
Eosinophils produced EXC4 after challenge with the proinflammatory agents LTC4, prostaglandin D2, and IL-5, demonstrating that EXC4 can be synthesized from the endogenous pool of arachidonic acid.
EXs induced increased permeability of endothelial cell monolayer in vitro, indicating that EXs can modulate and enhance vascular permeability, a hallmark of inflammation. In this model system, EXs were 100 times more potent than histamine and almost as potent as LTC4 and LTD4. Taken together, this article describes the formation of proinflammatory EXs, in particular in human eosinophils but also in human mast cells and nasal polyps.
Cord blood-derived mast cells and surgically removed nasal polyps from allergic subjects also produced EXC4. Incubation of eosinophils with arachidonic acid favored the production of EXC4, whereas challenge with calcium ionophore led to exclusive formation of LTC4.
Eosinophils produced EXC4 after challenge with the proinflammatory agents LTC4, prostaglandin D2, and IL-5, demonstrating that EXC4 can be synthesized from the endogenous pool of arachidonic acid.
EXs induced increased permeability of endothelial cell monolayer in vitro, indicating that EXs can modulate and enhance vascular permeability, a hallmark of inflammation. In this model system, EXs were 100 times more potent than histamine and almost as potent as LTC4 and LTD4. Taken together, this article describes the formation of proinflammatory EXs, in particular in human eosinophils but also in human mast cells and nasal polyps.
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