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Eur Respir J 2002; 20:1228-1232
Copyright ©ERS Journals Ltd 2002

Murine gammaherpes virus as a cofactor in the development of pulmonary fibrosis in bleomycin resistant mice

S.S. Lok1, Y. Haider1, D. Howell2, J.P. Stewart3, P.S. Hasleton2 and J.J. Egan4

1 North West Lung Research Centre, Wythenshawe Hospital, Southmoor Road, Manchester, 2 Raynes Institute, University College London, London, 3 Dept of Veterinary Pathology, University of Edinburgh, Summerhall, Edinburgh, and 4 The Mater Misericordiae Hospital, Eccles Street, Dublin, Ireland, UK

CORRESPONDENCE: J.J. Egan, Dept of Respiratory Medicine, The Mater Misericordiae Hospital, Eccles Street, Dublin 7, Ireland. Fax: 35 316605451. E-mail: jegan@mater.ie

Keywords: bleomycin, murine gammaherpes virus, pulmonary fibrosis

Received: August 21, 2001
Accepted March 22, 2002

Studies of human tissue have suggested an association between productive Epstein Barr virus and idiopathic pulmonary fibrosis (IPF). However, a pathogenic role for the virus has not been established. This study was undertaken to develop an animal model, which would explore the association between viral infection and pulmonary fibrosis.

BALB/c mice (n=30), resistant to bleomycin, were primed with murine gammaherpesvirus 68 and then given intraperitoneal bleomycin. The mice were sacrificed at 28 days after bleomycin and their lungs assessed histologically and biochemically. Lung pathology was scored 0–3 for fibrotic and inflammatory change.

BALB/c mice given virus and bleomycin showed more lung fibrosis (median score 2.2) compared to those given bleomycin alone (median 0), virus alone (median 0.2) or phosphate-buffered saline (PBS) control (median 0). Similarly mice given both virus and bleomycin showed more lung inflammation (median score 1.9) compared to those given bleomycin (median 0.5), virus (median 0.8), or PBS control (median 0.2). There was a significant difference in collagen content between the bleomycin and virus group (mean 1.86 mg) compared to the belomycin alone group (mean 1.52 mg).

These results suggest that virus alone does not result in pulmonary fibrosis but that replicating virus in the presence of an exogenous injury may promote the development of pulmonary fibrosis.




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