LAUSR

Purpose Effective treatment of idiopathic pulmonary fibrosis (IPF) is still difficult. Macrophages (Mφ) are closely related to IPF. M1 phenotype Mφ exhibit proinflammatory properties, M2 phenotype Mφ promote fibrogenesis. We found that pirfenidone (PFD), a representative medication of IPF, suppresses lung fibrosis through M2 polarization. Furthermore, liposomal clodronate (LC) is reported to suppress lung fibrosis by depleting Mφ. This study aimed to investigate the effects of combined LC and PFD on lung fibrosis and M2 Mφ polarization and populations. Method Rats were randomly divided into five groups: sham, bleomycin (BLM), PFD, LC, and PFD+LC. Following intratracheal instillation of BLM, rats were orally administered PFD daily. Rats were administered LC intravenously at 7 days and sacrificed at 14 days. Fibrosis and Mφ polarization and populations were analyzed in lung. Results Fibrosis and M2 marker levels were increased in BLM group, whereas PFD, LC, and PFD+LC groups showed significantly suppressed fibrosis and M2 markers. However, there were no synergistic effects of PFD+LC. Conclusion PFD or LC regulated lung fibrosis and M2 markers, but the suppressive effect on lung fibrosis and M2 Mφ polarization and populations was not be enhanced by the combination of PFD and LC.