Common denominator that triggers allergic asthma

15 Oct Common denominator that triggers allergic asthma

In recent decades, asthma has become a major public health problem. The exponential increase in asthma cases in industrialised countries over the past 50 years is due to major changes in our environment. Included in these environmental factors are excessive hygiene, ambient air pollution and respiratory viral infections, which are major risk factors for allergic asthma.

The mechanism by which different pro-allergic environments induce the development of asthma has remained largely unknown. However, in a study published in Nature Immunology, researchers have identified a common denominator.

Studying mice exposed to these different environmental factors it was found that neutrophils were being recruited into the lung and releasing networks of DNA fibres which cause allergic sensitisation, inflammation and asthma development. When the mice were treated with compounds that prevented the recruitment of these neutrophils into the lungs they were protected against disease development.

This discovery allows new therapeutic options to be considered in the prevention and treatment of allergic asthma. For example, a molecule already used in human medicine to treat cystic fibrosis, pulmozyme, could also be used to destroy the DNA released by neutrophils and prevent the development of asthma in people exposed to high-risk environments.

 

Story Source:

University of Liege. “Common denominator that triggers asthma in favorable environments.” ScienceDaily. ScienceDaily, 7 October 2019. <www.sciencedaily.com/releases/2019/10/191007180039.htm>.

 

Journal Reference:

Coraline Radermecker, Catherine Sabatel, Céline Vanwinge, Cecilia Ruscitti, Pauline Maréchal, Fabienne Perin, Joey Schyns, Natacha Rocks, Marie Toussaint, Didier Cataldo, Sebastian L Johnston, Fabrice Bureau, Thomas Marichal. Locally instructed CXCR4hi neutrophils trigger environment-driven allergic asthma through the release of neutrophil extracellular traps. Nature Immunology, 2019; DOI: 10.1038/s41590-019-0496-9