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Infection and Immunity, November 2003, p. 6213-6221, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6213-6221.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Absence of the Macrophage Mannose Receptor in Mice Does Not Increase Susceptibility to Pneumocystis carinii Infection In Vivo

Steve D. Swain,1* Sena J. Lee,2 Michel C. Nussenzweig,2 and Allen G. Harmsen1

Department of Veterinary Molecular Biology, Montana State University, Bozeman, Montana 59717,1 Laboratory of Molecular Immunology, Howard Hughes Medical Institute, The Rockefeller University, New York, New York 100212

Received 5 June 2003/ Returned for modification 14 July 2003/ Accepted 2 August 2003

Host defense against the opportunistic pathogen Pneumocystis carinii requires functional interactions of many cell types. Alveolar macrophages are presumed to be a vital host cell in the clearance of P. carinii, and the mechanisms of this interaction have come under scrutiny. The macrophage mannose receptor is believed to play an important role as a receptor involved in the binding and phagocytosis of P. carinii. Although there is in vitro evidence for this interaction, the in vivo role of this receptor in P. carinii clearance in unclear. Using a mouse model in which the mannose receptor has been deleted, we found that the absence of this receptor is not sufficient to allow infection by P. carinii in otherwise immunocompetent mice. Furthermore, when mice were rendered susceptible to P. carinii by CD4+ depletion, mannose receptor knockout mice (MR-KO) had pathogen loads equal to those of wild-type mice. However, the MR-KO mice exhibited a greater influx of phagocytes into the alveoli during infection. This was accompanied by increased pulmonary pathology in the MR-KO mice, as well as greater accumulation of glycoproteins in the alveoli (glycoproteins, including harmful hydrolytic enzymes, are normally cleared by the mannose receptor). We also found that the surface expression of the mannose receptor is not downregulated during P. carinii infection in wild-type mice. Our findings suggest that while the macrophage mannose receptor may be important in the recognition of P. carinii, in vivo, this mechanism may be redundant, and the absence of this receptor may be compensated for.

* Corresponding author. Mailing address: Department of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717. Phone: (406) 994-7691. Fax: (406) 994-4303. E-mail: uvsss{at}montana.edu.

Editor: T. R. Kozel

Infection and Immunity, November 2003, p. 6213-6221, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6213-6221.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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