Sensory neuroplasticity in asthma

Asthma is a chronic inflammatory disease characterized by airway hyperreactivity, partly driven by sensory neuron dysfunction. This dissertation introduces a novel whole-organ nerve visualization and quantification method to study neuroplasticity in asthma. Using this approach, we show that eosinophils promote branched outgrowth of airway nerves in chronic, but not acute, allergic inflammation, leading to increased reflex bronchoconstriction. Transgenic eosinophil-deficient mice confirmed eosinophil necessity for these changes. Similar eosinophil-driven neuroplasticity was observed in atopic dermatitis models and co-culture experiments. These findings reveal eosinophil-mediated neuroimmune interactions as key contributors to asthma morbidity and allergic disease pathogenesis.