Asthma is a chronic inflammatory disease of the respiratory system. The mucous membranes of the lungs of an asthmatic person tend to overproduce a sticky protein called mucin, which plugs small airways and prevent air from traveling through them, leaving the person gasping for air. Researchers at Houston Methodist in the United States have now uncovered the molecular mechanism that causes overproduction of mucin.

Epithelial cells in the lungs secrete mucin to keep the organs membranes moist to be able to absorb oxygen and to protect the membrane surface. In healthy lungs, the production of mucin is tightly controlled. Too much mucin is produced as a result of hyperactivity of white blood of the immune system called T helper cells in the lungs, according to the new study.

The T helper cells rally the the immune system when it recognises foreign toxins by secreting a protein called interleukin 9 or IL-9. In asthma, the T helper cells express a molecule called OX40, which activates regions of DNA called super-enhancers such that those genes are expressed that cause T helper cells to produce an abundance of IL-9. This triggers to massive production of mucin in the airways.

The finding, published in Journal of Experimental Medicine, can help design new drugs to treat asthma by targeting super-enhancers.