A new research suggests that sensory neurons are responsible for bronchial hyperactivity.
Asthma is a debilitating condition and cause of death for 250,000 people across the world each year. People with asthma have hyperactive airways and thickened lung walls blocked with mucus.
The condition can be fatal and during an asthma attack airways tighten even further in the presence of a trigger, such as pollen, dust mites or a viral infection. The present therapies treat asthma attacks as immune responses and focus on immune system suppression.
It has been well researched and observed that the immune system plays an important role in asthma. But, treatments holding back the immune response to relieve inflammation do not control asthma symptoms completely. This shows that asthma might involve an additional mechanism.
Researchers of this study found that this mechanism might be the nervous system activity. They arrived at the observation after genetically engineering mice with different groups of inactive neurons. The mice were given an allergy to ovalbumin, egg white protein. The allergy causes asthma like symptoms such as airway hyperactivity and constriction of the airways, they explained in press release.
The group of mice was exposed to ovalbumin. Researchers noted that all but one group of mice experienced allergy symptoms. In the asymptomatic mice, nerve cells that express a receptor called transient receptor potential vallinoid 1 (TRPV1) were inactive, the press release added.
The team stated that the mice did not exhibit asthma-like symptoms. However, their immune systems did respond to the allergen by producing ovalbumin-specific immunoglobulins and accumulated leukocytes in their lungs.
The study was been published in the journal Proceedings of the National Academy of Sciences.