A groundbreaking study has highlighted how psychological stress can directly influence lung inflammation in asthma patients, revealing intricate biological connections between the brain, immune system, and lungs. Conducted by neuroscientist Melissa Rosenkranz and her team at the University of Wisconsin-Madison, the research was recently published in Brain, Behavior, and Immunity and offers a fresh perspective on managing inflammatory diseases like asthma.
Rosenkranz has long been fascinated by the relationship between mental states and bodily function. “I’ve been really interested in wanting to understand the biology that is behind the connection between mind and body,” she said. This latest study takes a significant step toward decoding that relationship, focusing on how stress-related brain activity correlates with immune responses in the lungs.
The researchers recruited individuals with mild asthma and subjected them to the Trier Social Stress Test, a well-established method of inducing acute stress through public speaking and mental arithmetic. Participants then provided saliva samples to measure cortisol—a stress hormone—and underwent brain scans using positron emission tomography (PET). To complete the experiment, they were exposed to an inhaled allergen designed to provoke a mild asthmatic reaction, allowing scientists to assess inflammatory markers in their airways.
Interestingly, it wasn't the stress test alone that influenced lung function. Rather, individual differences in biological reactions to stress proved critical. Participants who showed higher cortisol levels also demonstrated increased activity in brain regions associated with fear and social stress. This, in turn, was linked to heightened expression of interleukin-23A (IL-23A) in the airways—an inflammatory protein associated with the Th17 immune pathway.
Traditionally, asthma has been linked with the Th2 immune pathway, but growing evidence points to a role for the Th17 pathway, previously known for its involvement in autoimmune disorders like lupus and rheumatoid arthritis. According to Rosenkranz, the new findings suggest that targeting the Th17 pathway may be a more effective treatment strategy for stress-sensitive asthma patients. “Maybe drugs that are able to modify immune responses in the Th17 pathway might be more effective,” she noted.
One of the challenges is that IL-17, another molecule in the Th17 pathway, can promote glucocorticoid resistance. This reduces the effectiveness of both natural cortisol and steroid-based asthma medications, making stress-induced inflammation particularly difficult to treat.
These insights align with Rosenkranz’s earlier work on psychological interventions such as mindfulness training. She now aims to investigate whether mindfulness could reduce stress-induced priming of the Th17 pathway, potentially restoring the effectiveness of traditional asthma medications.
Sonia Cavigelli, a behavioral neuroendocrinologist at Pennsylvania State University who was not involved in the study, praised the multidimensional approach. “They’re measuring biology at multiple levels—from brain activity to immune response to lung function,” she said.
Cavigelli also raised questions about how these mechanisms might differ across sexes, given well-documented differences in stress and immune responses. “I think we need to know that stuff, especially if we’re thinking about treatment,” she added.
This research marks a significant advance in understanding how stress exacerbates asthma and could pave the way for more tailored and effective treatments in the future. By bridging the gap between psychological states and physical health, Rosenkranz and her team offer new hope to asthma sufferers affected by chronic stress.
Source:https://www.the-scientist.com/researchers-uncover-mechanisms-linking-the-brain-and-lungs-in-asthma-73041
This is non-financial/medical advice and made using AI so could be wrong.