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Infection and Immunity, April 2004, p. 2140-2147, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2140-2147.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Effect of Bronchoalveolar Lavage Fluid from Pneumocystis carinii- Infected Hosts on Phagocytic Activity of Alveolar Macrophages

Mark E. Lasbury, Peimao Lin, Dennis Tschang, Pamela J. Durant, and Chao-Hung Lee*

Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202

Received 9 October 2003/ Returned for modification 20 November 2003/ Accepted 12 January 2004

Alveolar macrophages from Pneumocystis carinii-infected rats are defective in phagocytosis. To investigate whether this defect is due to a certain factor present in P. carinii-infected lungs, alveolar macrophages from uninfected rats were incubated with bronchoalveolar lavage (BAL) fluid samples from P. carinii-infected rats. Alveolar macrophages treated with these BAL fluid samples became defective in phagocytosis but remained normal when treated with BAL fluid samples from noninfected or Toxoplasma gondii-infected rats. The suppressive activity of the BAL fluid samples from P. carinii-infected rats on phagocytosis was retained when the BAL fluid samples were passed through a filter with a pore size of 0.45 µm but was lost when the BAL fluid samples were digested with proteases such as trypsin, pepsin, papain, or endopeptidase Gly-C. Lipid fractions of these BAL fluid samples had no suppressive activity on phagocytosis. The suppressive activity of these BAL fluid samples was also lost when they were incubated with concanavalin A-agarose beads, suggesting that the inhibitor is a glycoprotein. The inhibitor was estimated to be larger than 100,000 Da by exclusion filtration. After binding to the concanavalin A-agarose beads, the inhibitor in BAL fluid samples and P. carinii lysate could be eluted with 200 mM methylmannose. Treatment of both the crude BAL fluid samples and P. carinii lysate and the 200 mM methylmannose eluate with antibody against the major surface glycoprotein of P. carinii eliminated their suppressive activity. These results suggest that the factor capable of suppressing the phagocytic activity of alveolar macrophages is P. carinii major surface glycoprotein or one or more of its derivatives.

* Corresponding author. Mailing address: Department of Pathology & Laboratory Medicine, 1120 South Dr., FH 419, Indianapolis, IN 46202-5113. Phone: (317) 274-2596. Fax: (317) 278-0643. E-mail: chlee{at}iupui.edu.

Editor: T. R. Kozel

Infection and Immunity, April 2004, p. 2140-2147, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2140-2147.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Lasbury, M. E., Durant, P. J., Liao, C.-P., Lee, C.-H. (2009). Effects of Decreased Calmodulin Protein on the Survival Mechanisms of Alveolar Macrophages during Pneumocystis Pneumonia. Infect. Immun. 77: 3344-3354 [Abstract] [Full Text]  
  • Lasbury, M. E., Merali, S., Durant, P. J., Tschang, D., Ray, C. A., Lee, C.-H. (2007). Polyamine-mediated Apoptosis of Alveolar Macrophages during Pneumocystis Pneumonia. J. Biol. Chem. 282: 11009-11020 [Abstract] [Full Text]  
  • Lasbury, M. E., Durant, P. J., Ray, C. A., Tschang, D., Schwendener, R., Lee, C.-H. (2006). Suppression of Alveolar Macrophage Apoptosis Prolongs Survival of Rats and Mice with Pneumocystis Pneumonia.. J. Immunol. 176: 6443-6453 [Abstract] [Full Text]  


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