A new therapeutic target that could cure lung inflammation and injury has been identified by researchers at the University of Illinois, Chicago.
Acute respiratory distress syndrome, also known as ARDS, is an often fatal condition in which the lungs become swollen with water and protein, thereby making breathing almost impossible.
This often leads to death in 30 percent to 40 percent of cases.
The team has identified a new function of an enzyme that plays a vital role in the tissue injury in ARDS.
Previous studies had revealed that the enzyme, called non-musical myosin light-chain kinase, or MYLK, plays a crucial role in the disruption of the endothelial barrier, which thwarts water and protein build up in tissues.
According to Jingsong Xu, lead author of the paper and assistant professor in pharmacology and dermatology, as the enzyme disrupts endothelial barrier, a circulating blood cell, the neutrophil, "migrates into lung tissue and, when activated, can cause profound injury."
Neutrophils are white blood cells significant to immune system as they destroy invading bacteria and fungi. In ARDS, they misfire and attack healthy tissue.
"Although there have been many studies into how MYLK disrupts the endothelial barrier, no one has investigated how MYLK functions to regulate the neutrophil transmigration into tissues," We decided to look at this," Nature quoted Xu, as saying.
They found that MYLK drove neutrophils through the endothelial barrier.
The unexpected finding of a novel pathway "opens up a completely new set of possible therapeutic targets for the prevention and treatment of this deadly disease," said Dr. Asrar Malik, distinguished professor, head of pharmacology and co-author on the paper.
The study appears online in journal Nature Immunology.