FPR1 is expressed in nasal epithelial cells, lung epithelial cells, lung fibroblasts, and bronchoalveolar lavage fluid (BALF) cells45–48. The primary role of FPR1 in the respiratory tract is the promotion of wound healing or leukocyte migration to FPR1 ligands generated upon lung damage. As they can in the GI tract, the ligands of FPR1 can promote wound healing via FPR1 in epithelial cells of the respiratory tract. fMLP and AnxA1 activate alveolar basal epithelial cells and increase the expression of F-actin49. Mitochondrial formylated antigens stimulate wound healing in an FPR1-dependent manner. In particular, FPR1 is expressed in the lamellipodia of epithelial cells and directs the migration of these cells during the wound healing process47. Lung fibroblasts also migrate and express F-actin via FPR1 signaling. This process occurs through FPR1-mediated, calcium influx, PKC, and PI3K-dependent signaling pathways48. Bronchiolitis obliterans syndrome (BOS) is a fibroproliferative disorder caused by transplant rejection. In a murine BOS model, Fpr1 knockout mice showed attenuation of disease severity with decreased NF-κB nuclear translocation, MAPK signaling, and modulation of the NLRP3 inflammasome. The levels of cytokines directly related to fibrosis, such as VEGF and TGF-β, were also decreased in the Fpr1 knockout BOS mouse model50. These results suggest that FPR1 is detrimental in fibrotic diseases.