Can Certain Odors Worsen Airway Diseases? Researchers Think So

Can Certain Odors Worsen Airway Diseases? Researchers Think So

Olfactory receptors, a group of proteins that are activated by certain odors in the nose, can also be found in bronchi cells, where they regulate the way these cells work, according to a new study.

The authors argue that these proteins can explain why certain odors seem to worsen symptoms of airway diseases, such as asthma and chronic obstructive pulmonary disease (COPD), and could potentially become new therapeutic targets.

The study, “Olfactory Receptors Modulate Physiological Processes In Human Airway Smooth Muscle Cells,” was published in the journal Frontiers in Physiology by Benjamin Kalbe and colleagues from several research institutions in Germany.

The most widely known function of the olfactory receptors is smelling and detecting odors in the nose, but many studies have shown that these proteins are also present in other human tissues, where they contribute to several distinct functions. For this reason, Kalbe and his colleagues wondered whether these receptors could also play a role in airway functioning.

Using human muscle cells of the bronchial tissue, researchers observed that several odor molecules were able to trigger contractions in these cells. They also found that two olfactory receptors, OR1D2 and OR2AG1, were expressed in these cells.

However, these proteins had completely different effects when activated. OR2AG1, with an odorant compound called bourgeonal, inhibited cell contraction, whereas activation of OR1D2, with a odorant compound called amyl butyrate, increased cell contractility and the expression of inflammatory molecules (IL-8 and GM-CSF). The effects mediated by OR1D2 were inhibited by undecanal, a specific inhibitor of this protein.

These results suggest that in humans, OR1D2 activation may constrict the bronchi and promote inflammation, whereas OR2AG1 activation may help prevent airways from closing in response to pathological stimuli.

“Evidence suggests that perfumes can exacerbate asthma,” the authors wrote in their article. “Asthma is characterized by chronic airway inflammation that increases in severe and exacerbated asthma, and these changes are associated with IL-8 and GM-CSF hyperproduction in immunoactive airway cells.”

“Here, we demonstrated that bourgeonal (synthetic odor for lily of the valley, commonly used in perfumes) induces IL-8 and GM-CSF release from [bronchi cells]. These data are the first to indicate the influence of an odorant on the production of inflammatory cytokines in a lung cell type,” they wrote.

“IL-8 and GM-CSF also contribute to airway inflammation in stable and exacerbated COPD,” the researchers added. “Thus, our data suggest that exposure to distinct odorants might influence COPD and asthma pathogenesis.”

It’s possible that targeting these receptors may provide a good therapeutic strategy to treat chronic breathing disorders that constrict and obstruct the airways such as asthma, emphysema, and bronchitis.

“The best way would be to use a substance like amyl butyrate to support therapeutic intervention for patients with common airway diseases,” Kalbe said in a news release. “Amyl butyrate … might be a relaxing substance.”

The team is planning to explore the therapeutic potential of these receptors by using cells from people with chronic airway diseases to observe whether these receptors change in abundance or function in different disease states.

Researchers also want to understand whether the activation of these receptors is due to the presence of odorant molecules in the inhaled air, or if the body itself makes signaling molecules that regulate airway cells via these receptors.

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