A new culprit has been recognized that possibly plays a big role in the severity of asthma – a small protein chemokine called CCL26. These findings depict the first proof that CCL26 is a strong regulator of the migration of asthmatic eosinophils, normally observed in asthmatic airways. Results from this discovery may direct to new drug targets for the treatment of asthma.
Specifically, data from the report indicate that the chemokine CCL26 plays a crucial part in asthma pathogenesis and its severity by maintaining the recruitment of eosinophils early in the development of the disease and possibly later in serious asthma linked with prolonged lung eosinophilia. The researchers used blood from healthy and asthmatic subjects to seclude eosinophils and measure their migration response to CCL26 in vitro.
Researchers also evaluated their response to other chemokines, like CCL24, and CCL11, and showed that only CCL26 influenced an amplified eosinophil migration of asthmatic eosinophils compared to healthy cells. This additional migration happened after a 6-hour incubation and, in opposition to the migration induced by the other chemokines, was not destroyed by blocking the chemokine receptor CCR3 shared by these three chemokines.
The managing of eosinophils is central to asthmatic diseases and the underlying mechanisms are prime targets for treatments for the weakening and sometimes life-threatening symptoms of asthma and allergy. They also hope that, these studies will help to develop a new treatment that would specifically abolish bronchial inflammation and purvey a specific, efficacious and well-tolerated alternative to the current therapy.
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John Anderson completed his graduation in Biotechnology and also did PhD in Bio-pharmacology. He works as a medical consultant for kamagrasex.com