When we think of how we smell, we might envision odor molecules entering the nose and snuggly fitting into receptors that stimulate our brains into smelling, say, a certain brand of fabric softener. A sniff may even trigger a childhood memory. But scientists at Washington University in St. Louis and the University of Iowa have discovered that chemicals that we smell are detected by cells in our lungs as well. While cigarette smoke permeating the air, for example, elicits a pungeant smell in our brains, it can also prompt so-called neuroendocrine cells in our lungs to release a large amount of hormones that cause our airways to constrict. This is because the cells in our airways have the same odor receptors as our olfactory system, yet produce very different outcomes.
“We forget,” Ben-Shahar, author and leader of the study, told Washington University’s newsroom, “that our body plan is a tube within a tube, so our lungs and our gut are open to the external environment. Although they’re inside us, they’re actually part of our external layer. So they constantly suffer environmental insults,” he said, “and it makes sense that we evolved mechanisms to protect ourselves.”
The discovery of these so-called pulmonary neuroendocrine cells, or PNECs, was reported in the American Journal of Respiratory Cell and Molecular Biology and might be key in understanding respiratory diseases and their characteristic hypersensitivity to certain chemicals. Patients with chronic obstructive pulmonary disease (COPD), such as emphysema, suffer from frequent tightening of the chest, coughing, and wheezing when they are exposed to traffic fumes, pungent odors, perfumes, and other chemicals that can waft into their lungs.
Ben-Shahar hypothesized that future therapies could block odor receptors in our lungs, thereby short-circuiting respiratory attacks and reducing the need for steroids and dilators. “When people with airway disease have pathological responses to odors, they’re usually pretty fast and violent,” Ben-Shahar said to Washington University. “Patients suddenly shut down and can’t breathe, and these cells may explain why.”
As opposed to neurons in our nose that respond to odor molecules in a very specific manner, Ben-Sharar pointed out that PNECs in the lung are less discerning by having more than one kind of receptor. This means that several types of molecules can trigger a lung cell to spill out chemical messengers, namely serotonin and neuropeptides, to generate uncontrollable respiratory responses. “They are possibly designed,” he said, “to elicit a rapid, physiological response if you inhale something that is bad for you.”
Further proof that these lung cells serve as a potential target to stem respiratory disease comes from the authors noting that sufferers have more PNECs in their airway tissue than healthy donors. With lung doctors predicting higher rates of respiratory diseases thanks to global climate change and widespread allergies, Ben-Sharar is hopeful that his team’s findings bear therapeutic fruit.
Source: Ben-Sharar, Y. et al. Volatile-Sensing Functions for Pulmonary Neuroendocrine Cell. American Journal of Respiratory Cell and Molecular Biology. 2013.