By Henry Ehrlich
Because of the part it plays in the “new” food allergy, eosinophilic esophagitis (EoE), the eosinophil* inspires dread. This powerful white blood cell has long been associated with allergic asthma, the kind that responds to treatment with inhaled corticosteroids (ICS). As a matter of evolution, it is a powerful defense against parasites and it accumulates at sites in the body where the first-line defenders, mast cells and basophils, need back up. It’s one thing to know this about a cell and it’s another to see a description of how it actually works.
In a new article in JACI about biomarkers for asthma, which remains hard to diagnosis with precision for all the years it has been studied, I came across this:
On activation, eosinophils undergo respiratory burst, generating high levels of reactive oxygen species, eicosanoids, platelet-activating factor, and cytokines. Eosinophil peroxidase is unique in its ability to convert respiratory burst–generated hydrogen peroxide into hypobromous acid, a reactive brominating oxidant that modifies protein tyrosine residues forming urinary bromotyrosine (BrTyr). Thus BrTyr is a biochemical fingerprint of eosinophil activation, and this highly stable product can be detected in blood and urine.
As an occasional watcher of television news, the part that leapt out at me was “burst –generated hydrogen peroxide.” If hydrogen peroxide can turn the hair of television newscasters a uniform shade of glamor, what must it be doing to our tissue? The answer is, it remodels the lungs of asthmatics, and induces fibrostenosis in EoE patients. Blondes may have more fun, but asthmatics don’t. Take your medication and avoid your triggers.
*Discovered by the other Dr. Paul Ehrlich