Open Access Research

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

Claudia S Bitencourt1, Priscilla AT Pereira1, Simone G Ramos2, Suely V Sampaio1, Eliane C Arantes3, David M Aronoff4 and Lúcia H Faccioli1*

Author Affiliations

1 Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, 14040-903, Brazil

2 Departamento de Patologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, 14049-900, Brazil

3 Departamento de Física e Química, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, 14040-903, Brazil

4 Division of Infectious Diseases, Department of Internal Medicine, and the Department of Microbiology and Immunology, University of Michigan Health System, Ann Arbor, MI 48109, USA

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Fibrogenesis & Tissue Repair 2011, 4:3  doi:10.1186/1755-1536-4-3

Published: 13 January 2011

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.