Researchers have identified a molecule that prevents T-cells from triggering asthma brought on by allergens.
"We have identified a synthetic molecule, a sulfate monosaccharide, that inhibits the signal that recruits T-cells to the lungs to start an asthma attack," Minoru Fukuda, Ph.D., adjunct professor in the Tumor Microenvironment and Metastasis Program at Sanford-Burnham, said in a Sanford-Burnham Medical Research Institute news release."The molecule substantially lessened asthma symptoms such as inflammation, mucus production, and airway constriction."
The researchers made their findings using mouse models. The team found the synthetic sulfate monosaccharide prevents interactions between chemokine CCL20 (a " T-cell signaling protein") and heparin sulfate ("a molecule that protects and immobilizes CCL20 on epithelial cells in the lung") the news release reported.
The blocking of this interaction was found to prevent the recruitment inflammation-triggering T-cells.
Asthma affects more than 25 million Americans.
"There is currently no cure for asthma, and asthma control remains elusive for many patients, so there is still a need for research to find new therapies," Mike Tringale, senior vice president at the Asthma and Allergy Foundation of America (AAFA), a national asthma patient organization that has declared May National Asthma Awareness Month, said in the news release.
In the United States billions of dollars are spent every year on asthma medication. Despite these efforts a quarter of all emergency room visits in the U.S. are asthma-related. Asthma deaths have shot up 50 percent since 1980 in all age, gender, and racial groups. In children under the age of 19, the asthma death rate has increased by at least 80 percent since the year 1980.
"Pulmonary inhalation of this new molecule may help reduce asthma symptoms by suppressing chemokine-mediated inflammatory responses," Fukuda said. "We look forward to the further development of the molecule to treat the millions of people who suffer from this chronic disease."
