Abstract
Chlamydia trachomatis is the most common bacterial sexually transmitted disease in the world and specifically in the United States, with the highest incidence in age-groups 14–19 years. In a subset of females, the C. trachomatis genital infection leads to serious pathological sequelae including pelvic inflammatory disease, ectopic pregnancy, and infertility. Chlamydia pneumoniae, another member of the same genus, is a common cause of community acquired respiratory infection with significant number of children aged 5–14 yr displaying sero-conversion. Since these bacteriae share several antigenic determinants, we evaluated whether intranasal immunization with live C. pneumoniae (1×106 inclusion forming units; IFU) in 5 week old female C57BL/6 mice would induce cross-species protection against subsequent intravaginal challenge with Chlamydia muridarum (5×104 IFU), which causes a similar genital infection and pathology in mice as C. trachomatis in humans. Mice vaccinated intranasally with live C. pneumoniae, but not mock (PBS) immunized animals, displayed high levels of splenic cellular antigen-specific IFN-γ production and serum antibody response against C. muridarum and C. trachomatis. Mice vaccinated with C. pneumoniae displayed a significant reduction in the vaginal C. muridarum shedding as early as day 12 after secondary i.vag. challenge compared to PBS (mock) immunized mice. At day 19 after C. muridarum challenge, 100% of C. pneumoniae vaccinated mice had cleared the infection compared to none (0%) of the mock immunized mice, which cleared the infection by day 27. At day 80 after C. muridarum challenge, C. pneumoniae vaccinated mice displayed a significant reduction in the incidence (50%) and degree of hydrosalpinx compared to mock immunized animals (100%). These results suggest that respiratory C. pneumoniae infection induces accelerated chlamydial clearance and reduction of oviduct pathology following genital C. muridarum challenge, and may have important implications to the C. trachomatis-induced reproductive disease in humans.
Highlights
Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infection (STI), with approximately 90 million new cases detected annually worldwide [1]
While the aforementioned scenarios are fully plausible and likely contribute, we suggest that an additional distinct variable typically operational in human populations may be capable of affecting the course of C. trachomatis infection and pathological sequelae in human populations
Minimal IFN-c response was produced against chlamydial antigens by cells from mice immunized with PBS, and from cells obtained from C. pne, C. mur or PBS immunized groups incubated with the unrelated antigen bovine serum albumin (BSA), or media alone
Summary
Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infection (STI), with approximately 90 million new cases detected annually worldwide [1]. The greatest incidence of infection is in the 14–19 year age group [2]. The infection is treatable with available antimicrobials [1,3]. Repeated infections with the same or a different serovar occur commonly [4]. According to the Centers for Disease Control (2004), approximately 20–40% of women with past history of C. trachomatis infection(s) in the lower genital tract have been reported to develop serious sequelae such as pelvic inflammatory disease (PID). Subsets of patients with PID develop complications such as ectopic pregnancy and tubal infertility
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
