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Hyaluronidase recruits mesenchymal-like cells to the lung and ameliorates fibrosis.

Abstract
Hyaluronidases (HYALs) comprise a group of enzymes that degrade hyaluronic acid (HA). In this report, we reveal that a single intranasal inoculation of HYAL induces an increase in mononuclear cells within the bronchoalveolar space demonstrating a mesenchymal-like phenotype, expressing stem cell antigen-1 (SCA-1), CD44 and CD73 but not CD34, CD45, CD3, CD4, CD8 or CD19. This influx of mesenchymal stem cell (MSC)-like cells was dependent on leukotriene production within the lung parenchyma. These findings prompted experiments demonstrating that HYAL treatment potently blocked bleomycin-induced lung injury and fibrosis while decreasing transforming growth factor (TGF)-β production and collagen deposition. These data suggest that HYAL is a novel and promising tool to use autologous MSC-like cells in the treatment of pulmonary fibrosis.
AuthorsClaudia S Bitencourt, Priscilla At Pereira, Simone G Ramos, Suely V Sampaio, Eliane C Arantes, David M Aronoff, Lúcia H Faccioli
JournalFibrogenesis & tissue repair (Fibrogenesis Tissue Repair) Vol. 4 Issue 1 Pg. 3 (Jan 13 2011) ISSN: 1755-1536 [Electronic] England
PMID21232095 (Publication Type: Journal Article)

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