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Ghebremedhin, Anghesom; Salam, Ahmad Bin; Adu-Addai, Benjamin; Noonan, Steve; Stratton, Richard; Ahmed, Md Shakir Uddin; Khantwal, Chandra; Martin, George R.; Lin, Huixian; Andrews, Chris; Karanam, Balasubramanyam; Rudloff, Udo; Lopez, Henry; Jaynes, Jesse; Yates, Clayton

A Novel CD206 Targeting Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice

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  • Media type: E-Article
  • Title: A Novel CD206 Targeting Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice
  • Contributor: Ghebremedhin, Anghesom; Salam, Ahmad Bin; Adu-Addai, Benjamin; Noonan, Steve; Stratton, Richard; Ahmed, Md Shakir Uddin; Khantwal, Chandra; Martin, George R.; Lin, Huixian; Andrews, Chris; Karanam, Balasubramanyam; Rudloff, Udo; Lopez, Henry; Jaynes, Jesse; Yates, Clayton
  • imprint: MDPI AG, 2023
  • Published in: Cells
  • Language: English
  • DOI: 10.3390/cells12091254
  • ISSN: 2073-4409
  • Keywords: General Medicine
  • Origination:
  • Footnote:
  • Description: <jats:p>Activated M2-polarized macrophages are drivers of pulmonary fibrosis in several clinical scenarios, including Idiopathic Pulmonary Fibrosis (IPF). In this study, we investigated the effects of targeting the CD206 receptor in M2-like macrophages with a novel synthetic analogue of a naturally occurring Host Defense Peptide (HDP), RP-832c, to decrease profibrotic cytokines. RP-832c selectively binds to CD206 on M2-polarized bone marrow-derived macrophages (BMDM) in vitro, resulting in a time-dependent decrease in CD206 expression and a transient increase in M1-macrophage marker TNF-α. To elucidate the antifibrotic effects of RP-832c, we used a murine model of bleomycin (BLM)-induced early-stage pulmonary fibrosis. RP-832c significantly reduced fibrosis in a dose-dependent manner, and decreased CD206, TGF-β1, and α-SMA expression in mouse lungs. Similarly, in an established model of lung fibrosis, RP-832c significantly decreased lung fibrosis and significantly decreased inflammatory cytokines TNF-α, IL-6, IL-10, IFN-γ, CXCL1/2, and fibrosis markers TGF-β1 and MMP-13. In comparison with the FDA-approved drugs Nintedanib and Pirfenidone, RP-832c exhibited a similar reduction in fibrosis compared to Pirfenidone, and to a greater extent than Nintedanib, with no apparent toxicities observed. In summary, our findings showed that inhibiting the profibrotic alternatively activated M2-like macrophages using a novel peptide, RP-832c, could reduce BLM-induced pulmonary fibrosis in mice, warranting the therapeutic potential of this peptide for patients with pulmonary fibrosis.</jats:p>
  • Access State: Open Access