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Infection and Immunity, February 2003, p. 930-936, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.930-936.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Phagocytic Activity and Monocyte Chemotactic Protein Expression by Pulmonary Macrophages in Persistent Pulmonary Cryptococcosis

Wu He,1 Arturo Casadevall,2,3 Sunhee C. Lee,4 and David L. Goldman1*

Departments of Pediatrics,1 Medicine,2 Microbiology and Immunology,3 Neuropathology, Albert Einstein College of Medicine, Bronx, New York4

Received 5 August 2002/ Returned for modification 29 August 2002/ Accepted 28 October 2002

The mechanisms by which Cryptococcus neoformans persists in an immunocompetent host are not well understood. Using a rat model of persistent infection, we investigated the ability of pulmonary macrophages (PuM) to phagocytize C. neoformans and produce monocyte chemotactic protein 1 (MCP-1) as a function of the length of time of infection and opsonin. The ability of macrophages to affect serum-mediated phagocytosis varied over the course of infection and was dependent on CD11b/c and CD18 expression. Infection resulted in increased MCP-1 levels within the lung, though the actual amounts varied over the course of infection. Immunohistochemical studies localized MCP-1 expression to macrophages and epithelioid cells. Enhanced production of MCP-1 by PuM from infected rats was confirmed by ex vivo studies. Induction of MCP-1 following serum-mediated phagocytosis was observed for PuM from both infected and noninfected rats and depended on the interaction of C. neoformans with CD11b/c and CD18. Specific antibody was more efficient than serum in promoting phagocytosis and consistently elicited more MCP-1. The relative amount of MCP-1 produced in association with phagocytosis was similar for PuM at all lengths of time of infection. Decreased MCP-1 production was observed for PuM obtained from older rats, including long-term (8 to 10 months)-infected and age-matched controls, suggesting that aging may affect the production of MCP-1 by PuM in response to cryptococcal infection. In summary, our results show that macrophages are an important source of MCP-1 during pulmonary cryptococcosis and that MCP-1 production is actively regulated during infection. Furthermore, we find that phagocytosis of C. neoformans can serve as an important stimulus for MCP-1 production by PuM, though the efficiency of this process is dependent on the opsonin type and may be affected by aging.

* Corresponding author. Mailing address: Department of Pediatrics, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461. Phone: (718) 430-3766. Fax: (718) 430-8701. E-mail: dgoldma{at}aecom.yu.edu.

Editor: T. R. Kozel

Infection and Immunity, February 2003, p. 930-936, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.930-936.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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