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Infection and Immunity, January 2001, p. 24-33, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.24-33.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Surfactant Protein D Enhances Phagocytosis and Killing of Unencapsulated Phase Variants of Klebsiella pneumoniae

Itzhak Ofek,1 Adi Mesika,1 Moshe Kalina,1 Yona Keisari,1 Ranier Podschun,2 Hany Sahly,2 Donald Chang,3 David McGregor,3 and Erika Crouch3,*

Department of Human Microbiology, Tel Aviv University, Tel Aviv, Israel1; Department of Medical Microbiology and Virology, University of Kiel, Kiel Germany2; and Department of Pathology and Immunology, Washington University, St. Louis, Missouri3

Received 25 May 2000/Returned for modification 14 August 2000/Accepted 4 October 2000

Pulmonary surfactant protein D (SP-D) is a collagenous C-type lectin (collectin) that is secreted into the alveoli and distal airways of the lung. We have studied the interactions of SP-D and alveolar macrophages with Klebsiella pneumoniae, a common cause of nosocomial pneumonia. SP-D does not agglutinate encapsulated K. pneumoniae but selectively agglutinates spontaneous, unencapsulated phase variants, such as Klebsiella strain K50-3OF, through interactions with their lipopolysaccharides (LPS). These effects are calcium dependent and inhibited with maltose but not lactose, consistent with involvement of the SP-D carbohydrate recognition domain. Precoating of K50-3OF with SP-D enhances the phagocytosis and killing of these organisms by rat alveolar macrophages in cell culture and stimulates the production of nitric oxide by the NR-8383 rat alveolar macrophage cell line. SP-D similarly enhances the NO response to K50-3OF LPS adsorbed to Latex beads under conditions where soluble LPS or SP-D, or soluble complexes of SP-D and LPS, do not stimulate NO production. Our studies demonstrate that interactions of SP-D with exposed arrays of Klebsiella LPS on a particulate surface can enhance the host defense activities of alveolar macrophages and suggest that activation of macrophages by SP-D requires binding to microorganisms or other particulate ligands. Because unencapsulated phase variants are likely to be responsible for the initial stages of tissue invasion and infection, we speculate that SP-D-mediated agglutination and/or opsonization of K. pneumoniae is an important defense mechanism for this respiratory pathogen in otherwise healthy individuals.

* Corresponding author. Mailing address: Barnes-Jewish Hospital, North Campus, 216 S. Kingshighway, St. Louis, MO 63110. Phone: (314) 454-8462. Fax: (314) 454-5505. E-mail: crouch{at}path.wustl.edu.

Infection and Immunity, January 2001, p. 24-33, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.24-33.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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