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Infants born extremely preterm (<28 weeks gestation) have immature neural control of breathing and immature lungs, and thus immature lung-brain sensory axes. These sensory axes comprise molecularly distinct pulmonary vagal sensory neurons (PSNs). PSNs innervate distinct lung and brain regions, reflecting their unique roles in respiratory control. Moreover, single-cell RNA Sequencing indicates that PSNs are sensitive to common respiratory stimuli. Because of various pathological features in BPD and other common lung diseases, we are interested in understanding PSNs’ role in pathological nCOB, which often complicates BPD, COPD, and other lung diseases.

BPD is a consequence of exposure to mechanical ventilation and/or high oxygen therapy provided to infants born very premature (<28 weeks gestation). Contributing to the need for these therapies is an inability to properly control breathing. Similarly, breathing control is impaired in COPD contributing to COPD exacerbations. While this is known, there exist no therapies to modulate - in a targeted manner - breathing control. Unique subpopulations of vagal sensory neurons have been shown to have distinct effects on breathing. For example, Npy2r+ vagal neurons supposedly innervate alveoli and increase breathing in anesthetized mice. Given that alveoli are reduced in BPD, is this excitatory input also reduced? We seek to define the functional role of the various vagal afferent neuronal subtypes that innervate different lung regions in the context of BPD and COPD.