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Infection and Immunity, June 2003, p. 3384-3391, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3384-3391.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Prior Exposure to Live Mycobacterium bovis BCG Decreases Cryptococcus neoformans-Induced Lung Eosinophilia in a Gamma Interferon-Dependent Manner

Gerhard Walzl,1,{dagger} Ian R. Humphreys,1 Ben G. Marshall,2,{ddagger} Lorna Edwards,1 Peter J. M. Openshaw,2 Rory J. Shaw,3 and Tracy Hussell1*

Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine, London SW7 2AZ,1 National Heart and Lung Institute at St. Mary's Hospital, London W2 1PG,2 National Heart and Lung Institute at Hammersmith Hospital, London W12 OHS, United Kingdom3

Received 22 August 2002/ Returned for modification 2 November 2002/ Accepted 20 March 2003

Some common childhood infections appear to prevent the development of atopy and asthma. In some Mycobacterium bovis BCG-vaccinated populations, strong delayed-type hypersensitivity responses to mycobacterial antigens are associated with a reduced risk of atopy. Although BCG exposure decreases allergen-induced lung eosinophilia in animal models, little attention has been given to the effect of immunity to BCG on responses against live pathogens. We used the murine Cryptococcus neoformans infection model to investigate whether prior BCG infection can alter such responses. The present study shows that persistent pulmonary BCG infection of C57BL/6 mice induced an increase in gamma interferon, a reduction in interleukin-5, and a decrease in lung eosinophilia during subsequent Cryptococcus infection. This effect was long lasting, depended on the presence of live bacteria, and required persistence of mycobacterial infection in the lung. Reduction of eosinophilia was less prominent after infection with a mutant BCG strain ({Delta}hspR), which was rapidly cleared from the lungs. These observations have important implications for the development of vaccines designed to prevent Th2-mediated disease and indicate that prior lung BCG vaccination can alter the pattern of subsequent host inflammation.

* Corresponding author. Mailing address: Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine, SW7 2AZ London, United Kingdom. Phone: 44 207 5943091. Fax: 44 207 594 3095. E-mail: t.hussell{at}ic.ac.uk.

Editor: T. R. Kozel

{dagger} Present address: Medical Biochemistry, Faculty of Health Sciences, Stellenbosch University, Tygerberg 7505, South Africa.

{ddagger} Present address: Department of Respiratory Medicine, Southampton University Hospitals NHS Trust, Southampton, Hampshire SO16 6YT, United Kingdom.

Infection and Immunity, June 2003, p. 3384-3391, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3384-3391.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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