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

Departments of ¹Anatomy and Cell Biology and ²Obstetrics and Gynecology, University of Iowa College of Medicine, Iowa City, Iowa 52242; and ³Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110

Submitted 11 December 2003 ; accepted in final form 7 April 2004

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 C. trachomatis and C. pneumoniae but that SP-D only aggregates C. pneumoniae. In addition, we found that after phagocytosis in the presence of SP-A, the number of viable C. trachomatis pathogens in the THP-1 cells 48 h later was increased 3.5-fold. These findings suggest that SP-A and SP-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.

SP-A; SP-D; Chlamydia trachomatis; Chlamydia pneumoniae

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