A new study carried out by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham), the Max Planck Institute for Colloids and Interfaces (Germany), the Free University of Berlin (Germany), UC San Diego, and Shinshu University (Japan) has identified a novel molecule that prevents T-cells from orchestrating asthma brought on by allergens. The findings, published on May 12 in Proceedings of the National Academy of Sciences (PNAS), show promise for a new potent therapeutic agent to treat asthma, a chronic disease affecting more than 25 million Americans.
“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,” said Minoru Fukuda, Ph.D., adjunct professor in the Tumor Microenvironment and Metastasis Program at Sanford-Burnham. “The molecule substantially lessened asthma symptoms such as inflammation, mucus production, and airway constriction.”
The study, performed in mouse models for asthma research, showed that the synthetic sulfate monosaccharide blocks the interaction between chemokine CCL20—a T-cell signaling protein—and heparin sulfate, a molecule that protects and immobilizes CCL20 on epithelial cells in the lung. Blocking this interaction stalled the recruitment of the T-cells that trigger inflammation. The favorable results were achieved when the novel molecule was administered intravenously as well as by inhalation.
Although billions of dollars are spent every year on asthma medication, asthma still accounts for one-quarter of all emergency room visits in the U.S. each year (~1.75 million ER visits). And, asthma is on the rise. Since 1980, asthma death rates overall have increased more than 50 percent among all genders, age groups, and ethnic groups. The death rate for children under 19 years old has increased by nearly 80 percent since 1980.
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Source: Sanford Burnham Medical Research Institute
