Abstract
Groups of inbred female mice of strains CBA or C3H were infected genitally with a pathogenic human strain of Chlamydia trachomatis (N.I.1, serovar F) known to produce salpingitis and infertility in mice. Mice were inoculated under the ovarian bursa or directly into the uterine cavity with chlamydiae (test groups) or with sucrose-phosphate transport medium (control groups) before being challenged with chlamydiae by the same route 12-17 weeks later. Twenty-five pairs of test and control animals were killed from 7 to 77 days after challenge and oviductal inflammatory changes, recovery of organisms, and antibody responses were compared in the two groups. Salpingitis in the mice infected previously (tests groups) was more severe than in the controls in 56% of comparisons, the same in 24% and less severe in 20%. However, despite the increase in the severity of disease, shedding of C. trachomatis from the lower genital tract was less prolonged after rechallenge or did not occur. Salpingitis occurred in spite of the almost certain presence of pre-existing serum antibody, and accelerated and accentuated antibody response in the rechallenged mice. Furthermore, the continued existence of high titres of antibody was not associated with less severe disease. Thus, the results reveal that previous exposure to chlamydiae does not prevent salpingitis and suggest that its severity is influenced by cell-mediated immune mechanisms.
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Selected References
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