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Am J Physiol Lung Cell Mol Physiol (April 9, 2004). doi:10.1152/ajplung.00440.2003
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Submitted on December 11, 2003
Accepted on April 7, 2004

Surfactant proteins A and D enhance the phagocytosis of Chlamydia into THP-1 cells

Rebecca E. Oberley1, Kevin A. Ault2, Traci L. Neff2, Kavita R. Khubchandani1, Erika C. Crouch3, and Jeanne M. Snyder1*

1 Department of Anatomy and Cell Biology, The University of Iowa, Iowa City, IA, USA
2 Department of Obstetrics and Gynecology, The University of Iowa, Iowa City, IA, USA
3 Department of Pathology, Washington University School of Medicine, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: jeanne-snyder{at}uiowa.edu.

Chlamydiae are intracellular bacterial pathogens that infect mucosal surfaces, i.e., the epithelium of the lung, genital tract, and conjunctiva of the eye, as well as alveolar macrophages. In the present study, we show that pulmonary surfactant protein A (SP-A) and surfactant protein D (SP-D), lung collectins involved in innate host defense, enhance the phagocytosis of Chlamydia pneumoniae and Chlamydia trachomatis by THP-1 cells, a human monocyte/macrophage cell line. We also show that SP-A is able to aggregate both Chlamydia trachomatis and Chlamydia pneumoniae but that SP-D only aggregates Chlamydia pneumoniae. In addition, we found that after phagocytosis in the presence of SP-A, the number of viable Chlamydia trachomatis pathogens in the THP-1 cells 48 hours later was increased ~3.5 fold. These findings suggest that surfactant proteins A and D interact with chlamydial pathogens and enhance their phagocytosis into macrophages. In addition, the chlamydial pathogens internalized in the presence of collectins are able to grow and replicate in the THP-1 cells after phagocytosis.




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