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Theoretical molecular mechanism of the effects of wildfire smoke on pulmonary function. The working hypothesis is that both alveolar macrophages (AM) and lung epithelial cells directly interact with smoke particles. The combined responses result in production of key cytokines and alarmins that activate innate lymphoid cells (ILC2) and lung parenchyma resulting in tissue remodeling and an obstructive pathology (i.e., COPD, asthma).
