Infertility in mice infected genitally with a human strain of Chlamydia trachomatis

Abstract

Progesterone-treated C3H and TO mice were inoculated genitally with a human C. trachomatis strain, serovar E, designated N.I. 1 or with 2SP control medium. Of the C3H mice serving as controls 93% had litters by the end of a 6-month period compared to 31% of mice infected with chlamydiae. This infertility could not be explained by tubal occlusion, since the oviducts appeared normal at autopsy. Some of the mice were induced to superovulate. Eggs were never recovered from the oviducts on the inoculated sides of infertile mice although they were sometimes found in the lumen of the uninoculated oviducts. In contrast, eggs were recovered routinely from both oviducts of control mice. In addition, eggs and/or their accompanying cumulus cells could be seen in the periovarial space of mice inoculated with chlamydiae, indicating a failure of the transportation of eggs to the oviduct. This could explain the high incidence of ectopic pregnancies in women after chlamydial infection. No adverse effect on fertility was seen in TO mice inoculated genitally with strain N.I.1. Of the mice given 2SP medium, 73% had litters, but 87% of the mice inoculated with chlamydiae were also fertile. There was, however, a significantly greater variation in the birth weights of mice born to infected TO mothers than those born to control mice. This difference in the susceptibility of mouse strains suggests that a genetic predisposition should also be considered for man.

Chlamydia trachomatis infection of human fallopian tube organ cultures

“…trachomatis has been assumed to be similar to the events seen in C. trachomatis infection of animals or tissue culture and in vivo chlamydial conjunctival infection. Tuffrey and coworkers (Tuffrey & Taylor-Robinson, 198 1 ;Tuffrey et al, 1982Tuffrey et al, , 1984Tuffrey et al, , 1985Tuffrey et al, , 1986) developed a mouse model of chlamydial genital tract infection using a variety of human isolates of C. trachomatis. They found that infection was enhanced by progesterone, which is thought to maintain epithelial cells on the uterine surface.…”

Immune-mediated control of Chlamydia infection

“…The ability of the Chlamydia organisms to enter this physical barrier is influenced by the stage of the estrus cycle. Shedding of the endometrial epithelium during certain stages of this cycle can limit the ability of C. trachomatis to establish a robust infection (Tuffrey et al, 1986;Ramsey et al, 1999). Urethral samples of infected individuals also contain defensins that have been shown to inhibit C. trachomatis infection in vitro (Porter et al, 2005).…”

Genetic susceptibility to chlamydial salpingitis and subsequent infertility in mice

“…Sections were cut through various levels of the block and stained with haematoxylin and eosin. Inflammatory changes were graded from + to + + + as described by Tuffrey et al (1986a).…”

“…Although a range of HLA-linked diseases has been described in man, only sexually acquired reactive arthritis, some cases of which have a chlamydial aetiology (Keat et al, 1987), has been strongly associated with the HLA haplotype, B27 (Keat, 1986). We have developed a mouse model of chlamydial salpingitis (Tuffrey et al, 1986a) and infertility (Tuffrey et ai, 1986b) that lends itself to the investigation of possible genetic factors that might influence susceptibility to genital chlamydial infections. Many mouse strains are genetically defined and in this paper we report investigations of the natural susceptibility or resistance of several strains of mice to chlamydial salpingitis and infertility, with emphasis on embryo implantation.…”