The possibility of a long-term treatment for severe asthma is approaching. The credit goes to the results obtained (after over 10 years of work) by an immunology institute in the USA. The focus of the studies is a way to block the thickening of airway muscle tissue in patients.
How does this finding relate to chronic asthma?
In patients with chronic asthma, tissue remodeling occurs: the smooth muscle of the airways produces a thickening that progressively worsens the patient's breathing problems.
“Current treatments for asthma, even the most innovative ones, they mainly serve to suppress symptoms and reduce allergic inflammation,” he explains Haruka Miki, a researcher who worked on the study. “There is no treatment yet to eliminate asthma. Especially in its severe form, even when the inflammation is suppressed, the underlying airway hyperresponsiveness and airway remodeling remain.”
Ten years of work
In 2011 the discovery that gave rise to everything. Researchers at the La Jolla Institute for Immunology revealed that a certain immune molecule (called LIGHT) is the key to airway thickening in asthma patients. This protein, called LIGHT, is produced by T cells in large quantities when the body comes into contact with an allergen.
The La Jolla team has been looking for the mechanism of involvement of the LIGHT protein ever since, and now they seem to have found it. In the new study, published in the Journal of Allergy and Clinical Immunology (I link it here), the researchers examined two key receptors expressed on airway smooth muscle cells.
One of these two receptors (LTβR) is vital for tissue remodeling. The finding is that LIGHT molecules binding to LTβR receptors trigger the airway thickening seen in chronic asthma.
“When those cells in the lungs cannot express LTβR, all the hallmarks of the response associated with severe asthma disappear or are very limited.” This is what the senior author of the study said: Matthew Croft.
The prospects for the fight against asthma
While this finding doesn't immediately mean we should expect a new treatment for severe asthma in the next year (or the year after), it shows promise for future therapies that address structural airway problems associated with chronic conditions like this.
If a treatment could be found that prevents LIGHT proteins from binding to LTβR or reduces LTβR volumes in airway cells, one of the key physiological features of chronic asthma could be prevented. The La Jolla team is currently collaborating with a pharmaceutical company to explore the possibility of turning these findings into a drug treatment.
In summary, this finding offers hope that one day we will be able to effectively treat and even prevent airway remodeling in asthmatic patients. I look forward to reporting on further progress in this area.
