In a nutshell, NPY may be elevated in the airways in sinus diseases or in asthma. NPY is also one of few negative regulators of airway cilia beating (via NPY2R receptors and PKC). This paper shows the same NPY2R/PKC pathway reduces cilia bitter receptor NO, linking NPY with impaired innate defense.
Airway neuropeptides (NPY, VIP, SubP, etc.) have diverse effects via GPCRs on airway epithelial & immune cells. While likely important for airway physiology & pathophysiology, we still don't know enough about how they influence these cells. Because T2R bitter receptor signaling to eNOS and production of NO controls other responses (like macrophage phagocytosis), NPY (or related PP or PYY) may also reduce T2R-mediated responses in other tissues (but likely depends on NPYRs expressed there). How do other neuropeptides regulate T2R responses in the airway? Stay tuned.