Taste buds in lung cells help direct muscle movement

Through an accidental discovery, taste bud cells have been found on the surface of muscle cells in the lungs.

According to researchers at the University of Maryland School of Medicine and the Hopkins School of Public Health and School of Medicine, this may help advance the understanding of respiratory illnesses such as asthma and chronic obstructive pulmonary disease.

Led by Stephen Liggett of the University of Maryland School of Medicine, the group had initially found the taste receptors on smooth airway muscle cells when examining the cells for other G protein-coupled receptors.

In an article published in Nature Medicine, the researchers detail their work examining the responsiveness of the cells and receptors to bitter compounds and how they would play a role in airway constriction and related respiratory illnesses.

Taste receptors in the mouth are found in clusters as taste buds on the tongue, where they send signals to the brain based on the compounds they come in contact with in the mouth.

However, these receptors are not bundled on the surface of smooth airway muscle cells lining the bronchi, the larger passageways that air travels through when entering the lung.

These receptors are also not linked to the brain or any other part of the nervous system, yet their interaction with certain compounds does cause a reaction in the muscle cells.

The researchers initially expected that these receptors, specific for bitter-tasting compounds, would cause the muscle cells to contract when exposed to bitter compounds, leading to airway restrictions. As a defensive mechanism, this would protect the human body from threats such as plant toxins.

This group of receptors, TAS2Rs, consists of 25 different subtypes that are capable of recognizing numerous bitter-tasting compounds, creating a thorough network of receptors with some overlap that are able to recognize a wide array of toxins.

Thus, the researchers hypothesized that the interaction between bitter compounds and bitter taste receptors along smooth airway muscle would cause contraction.

However, to their surprise, the exact opposite occurred. When testing mouse models, cultured lung cells, and healthy lung tissues, the researchers found that exposure to bitter compounds, specifically chloroquine, denatonium, and quinine, caused the muscle cells to relax instead of contract.

Dose-response curves from the group’s experiment also suggest that a calcium signaling pathway is responsible for the physiological changes in the cells leading to the relaxation of the airways.

In addition, the response generated by exposure to these bitter compounds produced a greater response in relaxing the airway muscles effect than beta-agonists, bronchodilators that are currently used to treat respiratory illnesses.

With limited options currently available for those suffering from respiratory illnesses, the researchers conclude that while their discovery can lead to examination of new therapeutic treatments for respiratory illnesses, the evolutionary basis for the response of receptors on smooth airway muscles remains speculative.

Nonetheless, their markedly greater response in dilation compared to beta-agonists demonstrate their potential to more effectively treat respiratory illnesses.