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Is there a way to switch `off` asthma attacks? Scientists think so!
Asthma has been correlated with an overabundance of one type of immune cell called M2 macrophages in the lungs.
New Delhi: In what could be a huge relief to all asthma patients, a new study has revealed ways of switching off the painful asthma attacks.
Scientists from Johns Hopkins have identified a critical cellular "off" switch for the inflammatory immune response that contributes to lung-constricting asthma attacks.
The switch is composed of regulatory proteins that control an immune signaling pathway in cells.
The new study, which is published in the Journal of Biological Chemistry, points out that the overabundance of one type of immune cells (M2 macrophages) in the lungs is somewhat responsible for asthma attacks. The researchers have also noted that turning off the signaling pathway that activates the M2 cells could prevent allergic attacks.
"Asthma patients are constantly firing through this pathway because those proteins are stuck in the 'on' position, without proper control by other proteins that shut down this reaction," explained Nicola Heller, Ph.D., assistant professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine, in a press release.
Asthma has been correlated with an overabundance of one type of immune cell called M2 macrophages in the lungs.
In a nonasthmatic person, the M2 macrophages activate to clean up inhaled allergens and foreign particles, and then deactivate when the irritant is broken down.
However, in people with asthma, the M2 cells and the chemical signals they emit linger and call in other cells that cause inflammation that can trigger an asthma attack with the classic symptoms of difficulty breathing, wheezing and shortness of breath.
Over time, the lung is changed by secretions from the M2 cells, which cause the lung tissue to remodel itself, contributing to irreversible obstruction and poor lung function.
"If you prevent these cells from becoming the M2 type, you can potentially stop the continued inflammation and long-term structural changes," said Heller.
(With Agency Inputs)