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Infection and Immunity, July 2006, p. 3817-3824, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.00317-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

In Vivo Role of Dendritic Cells in a Murine Model of Pulmonary Cryptococcosis

Karen L. Wozniak,1 Jatin M. Vyas,2 and Stuart M. Levitz1*

Section of Infectious Diseases, Evans Memorial Department of Medicine, Boston University Medical Center, Boston, Massachusetts,1 Division of Infectious Disease, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts2

Received 24 February 2006/ Returned for modification 13 March 2006/ Accepted 4 April 2006

Dendritic cells (DC) have been shown to phagocytose and kill Cryptococcus neoformans in vitro and are believed to be important for inducing protective immunity against this organism. Exposure to C. neoformans occurs mainly by inhalation, and in this study we examined the in vivo interactions of C. neoformans with DC in the lung. Fluorescently labeled live C. neoformans and heat-killed C. neoformans were administered intranasally to C57BL/6 mice. At specific times postinoculation, mice were sacrificed, and lungs were removed. Single-cell suspensions of lung cells were prepared, stained, and analyzed by microscopy and flow cytometry. Within 2 h postinoculation, fluorescently labeled C. neoformans had been internalized by DC, macrophages, and neutrophils in the mouse lung. Additionally, lung DC from mice infected for 7 days showed increased expression of the maturation markers CD80, CD86, and major histocompatibility complex class II. Finally, ex vivo incubation of lung DC from infected mice with Cryptococcus-specific T cells resulted in increased interleukin-2 production compared to the production by DC from naïve mice, suggesting that there was antigen-specific T-cell activation. This study demonstrated that DC in the lung are capable of phagocytosing Cryptococcus in vivo and presenting antigen to C. neoformans-specific T cells ex vivo, suggesting that these cells have roles in innate and adaptive pulmonary defenses against cryptococcosis.

* Corresponding author. Mailing address: Section of Infectious Diseases, Boston University Medical Center, 650 Albany St., Boston, MA 02118. Phone: (617) 638-7904. Fax: (617) 638-7923. E-mail: slevitz{at}bu.edu.

Editor: A. Casadevall

Infection and Immunity, July 2006, p. 3817-3824, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.00317-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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