by Asthma treatment may be taking a new direction as scientists find a class of drugs that do not suppress the immune system’s response to infections such as influenza A.
According to the latest figures from the Australian Bureau of Statistics, just under 2.7 million (10.7%) Australians had asthma in 2020-21, with a third of sufferers using daily medication.
Treatments for allergic asthma – where the lungs become inflamed due to allergens such as dust mite droppings – are often through drugs that suppress the immune system which can lead to increased susceptibility to infections such as the flu.
An international team of medical researchers has investigated a new type of drug called a “calcium release-activated calcium channel blocker”, (CRAC). This compound blocks the action of calcium signals in immune cells and, in the lungs of mice, dramatically reduces inflammation and mucus accumulation when exposed to dust mite feces.
“Our study provides evidence that a new class of drugs targeting CRAC channels can be safely used to treat allergic asthma without creating vulnerability to infections», says senior study author Dr. Stefan Feske and Jeffrey Bergstein Professor of Medicine in the Department of Pathology at NYU Langone Health.
Allergic asthma is the result of an inappropriate inflammatory response to an irritant. For example, when an asthmatic who is allergic to dust mite feces inhales it, cytokines are produced by a special subset of T immune cells known as T helper (Th) 2 cells. These cytokines are small proteins that help exchange of cell-to-cell messages in immune responses, for example when the body needs to communicate to fight an infection.
Read more: Australian researchers make breakthrough in asthma
In allergic asthma responses, however, these cytokines promote the production of an antibody called IgE and encourage immune cells, called eosinophils, to travel to the lungs where they cause inflammation resulting in wheezing, shortness of breath, chest tightness and coughing.
In mice, the CRAC inhibitor, known as CM4620, worked to stop calcium from entering CRAC channels. This in turn stopped the T cells from becoming Th2 cells, stopping cytokine production and subsequent inflammation.
By investigating the immune response to influenza A viruses in their mouse models, the researchers were able to show that the CRAC inhibitor did not compromise immunity to the infection – a key concern for developing effective asthma therapies.
Co-first author Yin-Hu Wang, PhD, a postdoctoral fellow in the Feske lab, is positive about the new drug’s potential impact: “This points to CRAC channel inhibition as a promising, potential future treatment approach for allergic airway disease ».
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