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Infection and Immunity, January 2003, p. 437-445, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.437-445.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Normal Host Defense during Systemic Candidiasis in Mannose Receptor-Deficient Mice

Sena J. Lee,1 Nai-Ying Zheng,2 Monica Clavijo,1 and Michel C. Nussenzweig1*

Laboratory of Molecular Immunology, Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10021,1 Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 731042

Received 31 May 2002/ Returned for modification 30 June 2002/ Accepted 10 September 2002

Pathogen pattern recognition receptors (PRRs) recognize common structural and molecular motifs present on microbial surfaces and contribute to induction of innate immune responses. The mannose receptor (MR), a carbohydrate-binding receptor expressed on subsets of macrophages, is considered one such PRR. In vitro experiments have implicated the MR in phagocytosis of mannose-bearing microbes, including Candida albicans, and enhancement of antifungal response by macrophages. However, the significance of the MR's contribution to immune response during systemic C. albicans infection has never been directly demonstrated. Using MR-deficient mice in an in vivo infection experiment, we examined the role of the MR in immune response during disseminated candidiasis. MR-/- and wild-type control mice were challenged intraperitoneally with C. albicans, and the survival rates, tissue fungal burden, inflammatory cell recruitment, and specific antibody production after infection were evaluated. We found no significant difference in survival between the two mouse strains. MR-/- mice had higher average fungal burdens in some of the organs on days 7 and 21 but exhibited competence in inflammatory cell recruitment and antibody production. We also observed in vitro that MR-/- peritoneal cavity macrophages were equally capable of C. albicans uptake and that phagocytosis could be blocked with ß-glucan. We conclude that the MR is not required for the normal host defense during disseminated candidiasis or for the phagocytosis of C. albicans and that a ß-glucan receptor may be required for C. albicans phagocytosis.

* Corresponding author. Mailing address: Rockefeller University, 1230 York Ave., New York, NY 10021. Phone: (212) 327-8067. Fax: (212) 327-8370. E-mail: nussen{at}mail.rockefeller.edu.

Editor: T. R. Kozel

Infection and Immunity, January 2003, p. 437-445, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.437-445.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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