Fig. 1

Pulmonary Macrophages in health and disease: During homeostasis, AM helps in surfactant and cellular debris removal. Transcription factors such as PPAR-γ, ERG2, and BACH2 helps in maturation and differentiation of fetal monocytes that seeds alveolar space during embryonic stage. Together with signals such as GM-CSF, TGF-β, and neonatal derived 12-HETE, AM gain identity, with almost no input from circulatory monocytes. IM1 are also locally maintained, however, IM2 required monocytes for its maintenance. Following a respiratory virus infection, the pool of AM is partially depleted due to cell death. The lung compartment is later experienced CCR2 dependent influx of monocytes, which are later differentiated into monocyte derived alveolar macrophages (MoAM) that can drive lung inflammation and lung fibrosis. IM2 can be infected by respiratory viruses, which further amplify the inflammatory response