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Serum Amyloid P Therapeutically Attenuates Murine Bleomycin-Induced Pulmonary Fibrosis via Its Effects on Macrophages

2010; Public Library of Science; Volume: 5; Issue: 3 Linguagem: Inglês

10.1371/journal.pone.0009683

1932-6203

Lynne A. Murray, Rogério Silva Rosada, Ana Paula Moreira, Amrita Joshi, Michael S. Kramer, David P. Hesson, Rochelle L. Argentieri, Susan K. Mathai, Mridu Gulati, Erica L. Herzog, Cory M. Hogaboam,

Medical Imaging and Pathology Studies

Macrophages promote tissue remodeling but few mechanisms exist to modulate their activity during tissue fibrosis. Serum amyloid P (SAP), a member of the pentraxin family of proteins, signals through Fcgamma receptors which are known to affect macrophage activation. We determined that IPF/UIP patients have increased protein levels of several alternatively activated pro-fibrotic (M2) macrophage-associated proteins in the lung and monocytes from these patients show skewing towards an M2 macrophage phenotype. SAP therapeutically inhibits established bleomycin-induced pulmonary fibrosis, when administered systemically or locally to the lungs. The reduction in aberrant collagen deposition was associated with a reduction in M2 macrophages in the lung and increased IP10/CXCL10. These data highlight the role of macrophages in fibrotic lung disease, and demonstrate a therapeutic action of SAP on macrophages which may extend to many fibrotic indications caused by over-exuberant pro-fibrotic macrophage responses.