Asthma affects millions of people across the United States, making everyday activities like exercising, laughing, or even taking a deep breath difficult. Although treatments can help control symptoms, many people continue to experience flare-ups, highlighting the need for new approaches that address the disease at its source. Nicholas Jendzjowsky, PhD, investigator at The Lundquist Institute for Biomedical Innovation, aims to uncover an unexpected contributor to asthma: the communication between the nervous system and the immune system.
At the center of this study is immunoglobulin E (IgE), a type of antibody produced by the immune system. IgE plays an important role in protecting the body from parasites and certain harmful substances. However, in people with asthma and allergies, the immune system often produces too much IgE in response to otherwise harmless triggers such as pollen, mold, or dust. This excessive IgE sets off a chain reaction that causes inflammation, swelling, mucus production, and tightening of the airways—hallmarks of an asthma attack.
Scientists have long understood how IgE contributes to asthma, but they are still working to understand why the body produces too much of it in the first place. This project, recently funded by the National Institute of Health for $449,625 over two years, explores a surprising possibility: that sensory nerves may be helping drive the process.
While nerves are best known for carrying signals related to touch, pain, and temperature, researchers now know they also communicate with the immune system. During an asthma attack, sensory nerves become over-activated and release small signaling molecules called neuropeptides. One of these molecules, known as substance P, has already been linked to inflammation, but does it play an even larger role than previously thought?
Early findings from Dr. Jendzjowsky’s research are promising. In laboratory studies, mice that lacked sensory nerves produced significantly less substance P and lower levels of IgE after exposure to a common asthma trigger. When substance P was restored, the asthma-like symptoms returned. Similarly, mice genetically unable to produce substance P also generated less IgE than normal mice. Together, these findings suggest that substance P may act as an important messenger, encouraging immune cells to produce excessive amounts of IgE.
The next phase of the research will investigate exactly how this happens. Scientists will study how substance P influences B cells—the immune cells responsible for producing antibodies—and whether it changes how these cells develop and ultimately switch to making IgE. The Jendzjowsky Lab will conduct experiments using both mouse models and human immune cells to better understand this process and determine whether the same biological mechanisms occur in people.
Understanding this connection between the nervous system and the immune system could reshape how scientists think about asthma. Rather than focusing only on blocking inflammation after it begins, researchers hope to identify ways to interrupt the signals that trigger excessive IgE production in the first place. If successful, this approach could lead to entirely new types of treatments that target the disease earlier in the inflammatory process.