A tickle in the nose can help trigger a sneeze, expelling irritants and disease-causing pathogens. But the cellular pathways that control the sneeze reflex go far beyond the sinuses and have been poorly understood.
Sneezing is the most forceful and common way to spread infectious droplets from respiratory infections. Scientists first identified a sneeze-evoking region in the central nervous system more than 20 years ago, but little has been understood regarding how the sneeze reflex works at the cellular and molecular level.
A neuroscientist at Washington University in St. Louis had a personal quest to understand “sneezing” as her entire family suffered from seasonal allergies. She pursued a better understanding of the molecular receptors and interactions of sneezing, similar to the research that led to the 2021 Nobel Prize in Physiology of how we perceive our sense of smell and taste awarded to 2 US Scientists, that could one day help mitigate pathogen transmission, or treat infectious diseases especially those that are transmitted though “a sneeze”.
While prior research had identified a region in the brains of cats and humans that is active during sneezing, the exact pathways involved in turning a stimulus like pollen or spicy food into a sneeze remained unknown.
To study sneezing in more detail, the research team developed a new model by exposing mice to irritants such as histamine, the basic chemical causing itching and allergies, and capsaicin—a chemical in spicy peppers—and characterizing the physical properties of their resulting sneezes. Then, focusing on that previously discovered sneeze center, they attempted to map the neural pathway. Using a pain-relieving drug, the researchers desensitized nasal sensory fibers in mice known to be triggered by capsaicin. As a result, the animals stopped sneezing in response to irritants, implicating the neurons that make up these fibers in the sneeze pathway. Next, the team screened those neurons for the signaling molecules they released, revealing that a peptide called neuromedin B (NMB) binds to and activates neurons prompting them to fire electrical impulses to another region of the brain that controls exhalation. This pathway, the authors concluded, is necessary for sneezing. Mice engineered without NMB or without the complementary receptor in the SpV had a significantly reduced sneezing reflex. (Sneezing reflex is mediated by a peptidergic pathway from nose to brainstem). These experiments appear to be neatly done and will build on a growing interest in sensory biology over the last decade, she says, adding that “the interactions between the immune system and the nervous system really set the stage” for the current work. The team is now interested in other sneezes—such as the light-induced sneeze reflex—and are also studying sneezes as a defense mechanism against viruses. They recently infected mice lacking the ability to sneeze with influenza and saw that, compared with wildtype mice, the modified mice had more-severe symptoms. How such findings will translate to humans remains unknown, but the development of better control over sneezing could one day have clinical relevance. “Instead of using antihistamines, we would have other options.”
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