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Evidence That Neutrophil Elastase-Deficient Mice Are Resistant to Bleomycin-Induced Fibrosis*

Sarah E. Dunsmore, PhD; Jurgen Roes, PhD; Felix J. Chua, MD; Anthony W. Segal, PhD; Steven E. Mutsaers, PhD; Geoffrey J. Laurent, PhD
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*From the Centres for Molecular Medicine (Drs. Roes and Segal) and Respiratory Research (Drs. Dunsmore, Chua, Mutsaers, and Laurent), University College London, London, UK.

Correspondence to: Sarah E. Dunsmore, PhD, Centre for Respiratory Research, The Rayne Institute, University College London Medical School, 5 University St, London WC1E 6JJ, UK; e-mail: s.dunsmore@ucl.ac.uk



Chest. 2001;120(1_suppl):S35-S36. doi:10.1378/chest.120.1_suppl.S35
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Pulmonary fibrosis, a disease characterized by excess collagen deposition, may result from a variety of insults to the lung. Despite much progress in understanding the mechanisms of collagen synthesis and deposition in the lung, therapeutic agents for this disease are limited, and prognosis for patients with pulmonary fibrosis remains poor. Theories on the development of pulmonary fibrosis largely center on the hypothesis that in response to injury, inflammatory and immune cells, such as neutrophils, enter the lung and together with activated resident cells, release mediators that induce fibroblasts to proliferate and/or produce excess collagen.1 Indeed, increased numbers of neutrophils have been detected in lung lavage fluid2 and tissue3 from patients with pulmonary fibrosis as well as in animal models of the disease.4

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