Ever since discovering that bitter taste receptors are found in the airways1, we have been following this emerging area with an eye to how and why this is happening. Some of the initial research focused on cells that line our lung passages: these cells are covered in fine, small “hairs” called cilia which help to capture and eliminate harmful substances by constantly beating and pushing material up and out of the bronchial system. Scientists looked for genes in those cells that might have instructions for cell-surface receptors, to see if they were able to sense anything, and to their surprise discovered that these cilia-bearing lung cells had bitter taste receptors on their outside surface.
This in-and-of-itself was quite interesting, but what really surprised researchers a few years later was the discovery that, when stimulated, the bitter taste receptors in the lungs led to relaxation in airway smooth muscles, helping to keep lung passages open2. The apparent mechanism involves the cilia-bearing cells releasing a calcium-based signal into the local circulation which hyperpolarized the smooth muscle cells, making it harder for them to contract. Net result: dilation of the air passages.
It is becoming increasingly clear that our respiratory passages, from the nose to the lungs, are loaded with bitter taste receptors. Robert Lee and Noam Cohen at UPenn, for example, are researching bitter taste receptors in the sinus passages (where they apparently stimulate an innate immune response.)3 This is part of a broader realization that bitter taste receptors don’t just protect us from poison, but also may protect us from pathogens seeking to gain a foothold in our airways (and GI tracts) by sensing bitter-tasting molecules that these pathogens produce. As a result, we are starting to take a broader view of bitter taste receptors as a more general protective, chemosensory mechanism that activates immunity, detoxification, and balanced metabolism.4 Doctors Lee and Cohen even noticed, upon digging further, that individuals with mutations in the structure of their bitter taste receptors may be more likely to experience challenge in their airways.5
Now, we have new research showing what occurs when those bitter taste receptors in the lungs are stimulated. Researchers in Spain discovered that, while there is overall airway dilation in response to bitter taste receptor stimulation, there is also a strong effect on the rate of beating and movement of the cilia cells that line our bronchial passages – in some cases, they become twice as active.6 This means that not only are the lung passages more dilated, there is also an increased rate of what we call “insensible” expectoration: the body’s natural process of moving material up and out of the lungs.
Though researchers at UPenn are exploring what this mean for those who suffer from chronic sinusitis, it is still too early to make broad claims about the role of bitter plants in maintaining optimal airway health. But it is exciting to think that bitter plants may have a role to play in helping the airway to maintain a normal, relaxed tone and a healthy level of mucus clearance.
1. Shah, Alok S., et al. "Motile cilia of human airway epithelia are chemosensory." Science 325.5944 (2009): 1131-1134.
2. Deshpande, Deepak A., et al. "Bitter taste receptors on airway smooth muscle bronchodilate by localized calcium signaling and reverse obstruction." Nature medicine 16.11 (2010): 1299-1304.
3. Lee, Robert J., and Noam A. Cohen. "Bitter and sweet taste receptors in the respiratory epithelium in health and disease." Journal of Molecular Medicine92.12 (2014): 1235-1244.
4. Prince, Alice. "The bitter taste of infection." The Journal of clinical investigation 122.11 (2012): 3847-3849.
5. Lee, Robert J., et al. "T2R38 taste receptor polymorphisms underlie susceptibility to upper respiratory infection." The Journal of clinical investigation 122.11 (2012): 4145-4159.
6. Ortiz, Jose Luis, et al. "Evaluation of Mucociliary Clearance by Three Dimension Micro-CT-SPECT in Guinea Pig: Role of Bitter Taste Agonists." PloS one 11.10 (2016): e0164399.