A new study published in the Journal of Leukocyte Biology reports on the finding of a small protein chemokine called CCL26 that acts as a potent regulator of the migration of asthmatic eosinophils, which are usually found in asthmatic airways. This discovery can be used in the development of new drugs for treating asthma.
"We hope that these studies will help to develop a new treatment that would specifically abrogate bronchial inflammation and provide a specific, efficacious and well-tolerated alternative to the current therapy," said Michel Laviolette, M.D., a researcher involved in the work from the Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec, Faculté de Médecine, Université Laval, Québec, Canada.
AdvertisementSpecifically, data from the report suggest that the chemokine CCL26 plays a crucial role in asthma pathogenesis and its severity by supporting the recruitment of eosinophils early in the development of the disease, and possibly later in severe asthma associated with persisting lung eosinophilia. To make this discovery, scientists used blood from healthy and asthmatic subjects to isolate eosinophils and measure their migration response to CCL26 in vitro. Researchers also assessed their response to other chemokines, CCL11 and CCL24, and showed that only CCL26 induced an amplified eosinophil migration of asthmatic eosinophils compared to healthy cells. Interestingly, this additional migration occurred after a 6-hour incubation and, in contrast to the migration induced by the other chemokines, was not eradicated by blocking the chemokine receptor CCR3 shared by these three chemokines.
"The control of eosinophils is central to asthmatic diseases and the underlying mechanisms are prime targets for treatments for the debilitating and sometimes life-threatening symptoms of asthma and allergy," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "This report shows that CCL26 could be a novel drug target to regulate eosinophils in these diseases."