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University of Calgary researchers have made a groundbreaking discovery: the lungs communicate directly with the brain during infections, playing a critical role in triggering symptoms of sickness. This finding challenges previous notions and may revolutionize the way we approach treating respiratory infections and chronic conditions.
Dr. Bryan Yipp, clinician researcher at the Cumming School of Medicine and senior author of the study, explains, “The lungs are using the same sensors and neurons in the pain pathway to let the brain know there’s an infection.” The brain then prompts the symptoms associated with sickness, such as fatigue, loss of appetite, and an overall feeling of being unwell. This revelation suggests that treating respiratory infections may require addressing not only the infection itself but also the nervous system.
Previously, it was believed that infections in the lungs and pneumonia triggered symptoms through inflammatory molecules reaching the brain via the bloodstream. However, findings from the study, conducted in mice, indicate that sickness results from direct activation of the nervous system in the lung.
Understanding this lung-brain dialogue is crucial for treatment, especially since bacteria causing lung infections can produce a biofilm, hiding from the nervous system and leading to less symptomatic infections. This discovery sheds light on phenomena like “happy hypoxia,” observed in COVID-19 patients who experience low oxygen levels without significant symptoms.
Dr. Yipp suggests that understanding lung-brain communication pathways may also benefit individuals with chronic lung infections like cystic fibrosis, where biofilm bacteria can cause asymptomatic periods followed by severe illness flares.
Published in Cell, the study involved an interdisciplinary team of experts in neurobiology, microbiology, immunology, and infectious disease. Drs. Christophe Altier, Joe Harrison, and Deborah Kurrasch from the University of Calgary, along with Dr. Jaideep Bains from the Krembil Research Institute, Toronto, are corresponding authors on the study.
One notable finding was that male mice were much sicker than females despite having the same infection. This difference was attributed to male sickness being more dependent on neuronal communications. This finding may provide insight into the colloquially termed “man flu,” suggesting that men may indeed experience more severe sickness due to respiratory infections.
The study’s findings highlight the interconnectedness of organs and the brain, suggesting new avenues for treating infections and their associated symptoms by targeting neurocircuitry alongside antibiotics. This research opens doors to a deeper understanding of disease and potential novel treatment approaches.
