Rationale: Although lung macrophages (M?) correlate with pulmonary fibrosis (PF) pathogenesis, the effect of pulmonary M? transplantation (PMT) on PF remains unclear. Aim: This study aimed to evaluate the effect of PMT on PF. Methods: Bone marrow (BM) mononuclear cells of wild-type (WT) mice were cultured in vitro to prepare BM-derived M?s (BMDM). BMDM or PBS were administered intratracheally 7 days after bleomycin (BLM) or PBS administration in WT mice. The four defined groups were P(PBS)+P, P+M(BMDM), B(BLM)+P, and B+M. We analyzed pulmonary inflammation and fibrosis-related gene expression on day 21. We performed lineage tracing of BMDM in CAG-EGFP mice by flow cytometry (FCM) and examined the location and morphology of BMDM using histopathological images. Results: The total cell counts, fibrosis score, and collagen deposition were higher in the B+M group than in the B+P. The Mcp-1 and Il-13 gene expression in the lung and Arg-1 and Il-10 in the alveolar M? (AM) of the B+M group were higher than those of the B+P. Such differences were not observed between the P+P and P+M groups. FCM analysis showed that the numbers of AM, interstitial M?s, monocytes, and dendritic cells significantly increased in the B+M group compared to those in the B+P. Moreover, the number of GFP⁺ cells in AM was lower in the B+M group than in the P+M. Histopathologically, GFP⁺ cells were F4/80⁺ and mainly accumulated in the inflammatory lesions in the B+M group. These results suggest that the fibrotic lung environment alters the function of BMDM, leading to the augmentation of inflammation and fibrotic gene expression. Conclusion: PMT may augment BLM-induced lung fibrosis in mice by exacerbating multifaceted inflammation.