Researchers found that lung immune cells (phagocytes) produce increased levels of neuropeptide Y (NPY) when mice are infected with severe influenza virus. NPY and its receptor form the NPY-Y1R axis. In mice with influenza, activation of this axis causes excess pulmonary inflammation and viral replication, leading to increased disease severity. Deactivation of NPY, Y1R or their downstream effects was found to mitigate disease severity. These pathways could be targets for novel anti-influenza medicines.
Lung neuropeptide exacerbates lethal influenza virus infection
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