February 28, 2013
Molecule That Decreases Airway Inflammation Could Lead To New Asthma Treatments
redOrbit Staff & Wire Reports - Your Universe Online
Researchers at the Brigham and Women´s Hospital (BWH) in Boston have discovered a molecule that controls cells responsible for decreasing airway inflammation in asthma patients, and their discovery could lead to new treatments for the millions of Americans that suffer from the disease.The molecule is known as lipoxin A4, and according to the researchers, it is responsible for resolving inflammation. It accomplishes this in two ways using two different types of immune cells. It encourages natural killer cells to decrease inflammation by working to facilitate eosinophil cell death. Lipoxin A4 also discourages type 2 innate lymphoid cells from promoting inflammation by prohibiting the secretion of cell-signaling molecules called interleukin-13.
As part of their research, which was published Wednesday in the journal Science Translational Medicine, the BWH team studied the lungs and blood of 22 subjects suffering from mild to severe asthma. They discovered the important roles that the natural killer cells and the type 2 innate lymphoid cells played in airway inflammation in those participants with a severe form of the respiratory condition.
“Stopping airway inflammation is similar to putting out a forest fire," senior study author Bruce Levy, MD of the BWH Department of Internal Medicine´s Pulmonary and Critical Care Medicine Division, said in a statement. "Firefighters tackle forest fires in two ways — dousing the fire with water and clearing away dry brush that could fuel the fire.”
“Lipoxin A4 does just that to resolve inflammation,” he added. “It is an airway inflammation fighter that performs the double duty of dampening pathways that ignite inflammation while at the same time clearing away cells that fuel inflammation.”
Levy and his colleagues had completed previous research that found patients with severe asthma also demonstrated a deficiency in lipoxin A4 production. That discovery, combined with the findings of their recent study, could help provide researchers and pharmaceutical firms with a new approach to treating the disorder — developing cutting-edge treatments designed to boost the molecule in those suffering from severe asthma symptoms.
“Most patients with severe asthma have chronic airway inflammation that never fully resolves,” Levy said. “This can lead to daily and often disabling symptoms despite available therapies. Our study provides new information on cellular targets that regulate inflammation and will enable the development of lipoxin-based therapeutics to decrease chronic inflammation in asthma and other diseases.”