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Infection and Immunity, December 2005, p. 8317-8321, Vol. 73, No. 12
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.12.8317-8321.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Department of Molecular Biotechnology, Ghent University, Ghent, Belgium,1 Department of Pathology, Bacteriology, and Poultry Disease, Ghent University, Merelbeke, Belgium,2 Laboratory of Immunogenetics, VU University Medical Centre, Amsterdam, The Netherlands,3 Department of Virology, Parasitology, and Immunology, Ghent University, Merelbeke, Belgium4
Received 22 October 2004/ Returned for modification 16 December 2004/ Accepted 16 August 2005
The purpose of the present study was to evaluate pigs as a large-animal model for female genital infection with two Chlamydia trachomatis human serovar E strains. Sixteen-week-old specific-pathogen-free female pigs (gilts) were intravaginally infected with the trachoma type E reference strain Bour or the urogenital serovar E strain 468. Several conclusions can be drawn from our findings on the pathogenicity of a primary C. trachomatis genital infection in gilts. First of all, we demonstrated that the serovar E strains Bour and 468 could ascend in the genital tract of gilts. The serovar E strains could replicate in the superficial columnar cervical epithelium and in the superficial epithelial layer of the uterus, which are known to be the specific target sites for a C. trachomatis genital infection in women. Second, inflammation and pathology occurred at the replication sites. Third, the organisms could trigger a humoral immune response, as demonstrated by the presence of immunoglobulin M (IgM), IgG, and IgA in both serum and genital secretion samples. Our findings imply that the pig model might be useful for studying the pathology, pathogenesis, and immune response to a C. trachomatis infection of the genital system.
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