Known as lipoxin A4, the molecule is responsible for resolving inflammation, and accomplishes this in two ways using two different types of immune cells. According to the researchers, lipoxin A4 first works by encouraging your natural killer cells to decrease inflammation, by working to facilitate eosinophil cell death. Then, the molecule prohibits the secretion of your cell-signaling molecules, called interleukin-13, which discourages type 2 innate lymphoid cells from promoting inflammation.
For the study, which is published in the journal Science Translational Medicine, 22 subjects whose wellness is affected by mild to severe asthma participated. The BWH team studied the lungs and blood of these patients, discovering the important roles that the natural killer cells and the type 2 innate lymphoid cells play in airway inflammation in the participants with a more severe form of the respiratory condition.
In a statement, senior study author Bruce Levy, MD of the BWH Department of Internal Medicine’s Pulmonary and Critical Care Medicine Division, explained, ‘Stopping airway inflammation is similar to putting out a forest fire. Fire-fighters tackle forest fires in two ways – dousing the fire with water and clearing away dry brush that could fuel the fire.’ He continued, ‘Lipoxin A4 does just that to resolve inflammation. 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.’
During previous research, Levy and his colleagues also discovered that found patients with severe asthma tend to demonstrate a deficiency in lipoxin A4 production. Thus, combined with the findings of their recent study, the team has laid the platform for researchers and pharmaceutical firms to build upon and develop a new approach to treating the disorder. The hope is that scientists will now be able to develop 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.’