Chloroquine and quinine - which are both used to flavor tonic water - prevented airway inflammation and other characteristics of allergic asthma in mice.
Researchers from the U.S. and Australia reveal how chloroquine and quinine prevented the development of allergic asthma in mice by activating the rodents' bitter taste receptors.
Chloroquine and quinine are compounds that are used to treat malaria, and they are also added to tonic water in order to give the beverage its distinctive, bitter taste.
Dr. Pawan Sharma, of the Woolcock Institute of Medical Research and School of Life Sciences at the University of Technology in Australia, and colleagues recently published their findings in the journal Scientific Reports.
Asthma is estimated to affect around 26 million children and adults in the U.S. The most common form of asthma is allergic asthma, which is triggered by exposure to dust mites, pollen, pet dander, mold, and other substances.
Inhaling such substances can lead to inflammation of the airways, causing symptoms such as shortness of breath, wheezing, coughing, and chest pain.
While there are medications that can help patients to manage their asthma symptoms - such as corticosteroids and beta2 agonists - Dr. Sharma notes that there are currently no asthma medications that target disease progression.
"Our current research on taste receptors is crucial in identifying new classes of drugs that can be an effective asthma treatment option in future," he adds.
Chloroquine and quinine prevented airway inflammation in mice
According to Dr. Sharma and colleagues, previous research found that activating bitter taste receptors on the tongue, called TAS2Rs, led to the relaxation of smooth muscle in the airways of asthma mouse models.
The new study aimed to build on those findings by assessing whether TAS2R agonists - that is, compounds that stimulate the bitter taste receptors - have the potential to reduce some of the key features of asthma.
To reach their findings, the researchers gave mouse models of allergic asthma intranasal doses of either chloroquine or quinine.
Twenty-four hours after administration, the lung function, airway inflammation, and airway structure of the mice were assessed upon exposure to two allergens.
Not only did chloroquine and quinine prevent airway inflammation in the mice, but the bitter compounds also prevented other key characteristics of allergic asthma, including mucus accumulation and structural changes to the airway.
The researchers also tested chloroquine and quinine on human airway cells. They found that the compounds block the chemotaxis, or movement, of immune cells in the airway in response to allergens, which helps to prevent airway inflammation.
Dr. Sharma and team note that further studies are needed in order to identify TAS2R agonists with higher efficacy for the treatment of asthma. "Alternately, existing drugs could be repurposed for asthma therapy," say the researchers, adding that:
"Advances in medicinal chemistry and computational modeling should catalyze the drug discovery process in exploiting TAS2Rs as novel anti-asthma therapeutic target."