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Infection and Immunity, October 2001, p. 6165-6171, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6165-6171.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Increase of gamma delta T Lymphocytes in Murine Lungs Occurs during Recovery from Pulmonary Infection by Nocardia asteroides

Stanley Tam,1 Donald P. King,2 and Blaine L. Beaman1,*

Department of Medical Microbiology and Immunology, University of California School of Medicine,1 and Department of Pathology, Microbiology and Immunology, University of California School of Veterinary Medicine,2 Davis, California 95616

Received 6 April 2001/Returned for modification 24 May 2001/Accepted 7 July 2001

Previous studies have demonstrated that gamma delta T lymphocytes are important for host resistance to pulmonary infection of the murine lung by log-phase cells of Nocardia asteroides. To study the role of gamma delta T cells in nocardial interactions in the murine lung, C57BL/6J wild type and C57BL/6J-Tcrd (gamma delta T-cell knockout mice) were infected intranasally with log-phase cells of N. asteroides GUH-2. At 3, 5, and 7 days after infection, the gamma delta T cells were quantified by multiparameter flow cytometry. At the same time, Gram and hematoxylin-eosin stains of paraffin sections were performed to monitor the host responses. The data showed that gamma delta T lymphocytes increased significantly within the lungs after intranasal infection, and the peak of this cellular increase occurred at 5 days. Furthermore, at this time, greater than 50% of the CD3 T-cell receptor (TCR)-positive (CD3+) cells were gamma delta TCR positive. Histological examination clearly showed divergent inflammatory responses in the lungs of wild-type mice compared to gamma delta T-cell knockout mice. The C57BL/6J-Tcrd mice were less capable of clearing the organism, and the polymorphonuclear leukocyte response lasted longer than in wild-type C57BL/6J mice. These results showed that gamma delta T cells were actively involved in modulating the innate host responses to murine pulmonary infection by N. asteroides.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, University of California School of Medicine, Davis, CA 95616. Phone: (530) 752-9663. Fax: (530) 752- 8692. E-mail: blbeaman{at}ucdavis.edu.

Infection and Immunity, October 2001, p. 6165-6171, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6165-6171.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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