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Genetic susceptibility to chlamydial salpingitis and subsequent infertility in mice
M Tuffrey1, F Alexander, C Woods
1Division of Sexually Transmitted Diseases, Clinical Research Centre, Harrow, Middlesex, UK.
Abstract:
Groups of mice from genetically defined inbred strains were infected genitally with a pathogenic human strain of Chlamydia trachomatis and their subsequent fertility was compared. The CBA, C3H (H-2o) and C3H/He-mg (H-2k) mice were less fertile than control mice, at least up to 6 months after infection. In contrast, fertility was not impaired in BALB/c mice or in congenic BALB/K mice, which had the H-2k haplotype. Reduced fertility was paralleled by the extent of histological oviductal inflammation in mice of each strain. No salpingitis was seen 21 days after infection in the BALB strains, but lesions were apparent in CBA and C3H strains up to about 70 days after inoculation and these sometimes developed into hydrosalpinges. These results indicate that susceptibility to chlamydial salpingitis and subsequent infertility is under genetic control. This control was not simply associated with the major H-2 gene complex, as mouse strains of the same haplotype (H-2k) differed in susceptibility. The fertility of BALB/c (H-2d) and BALB/K (H-2k) strains was no different from that of controls, and congenic C3H mice of differing H-2 haplotypes (H-2k and H-2o) showed reduced fertility. Although all the infected F1 (BALB/K x C3H/He-mg) mice produced litters at the same rate as untreated controls, the litters were considerably smaller. This was due to the occurrence of unilateral pregnancies in the mice inoculated under the ovarian bursae and possibly also to early fetal death in mice inoculated directly in the uterus. These findings emphasize the importance of early diagnosis and treatment of infection of the lower genital tract of women.
Insights
Genetic factors influence susceptibility to Chlamydia trachomatis infection, impacting mouse fertility and oviductal inflammation. Different mouse strains show varied responses, highlighting the genetic control over chlamydial salpingitis and infertility.
Area of Science:
- Immunology
- Genetics
- Reproductive Biology
Background:
- Chlamydia trachomatis is a significant cause of genital infections in humans.
- Genital Chlamydia trachomatis infections can lead to infertility.
- The role of host genetics in susceptibility to Chlamydia trachomatis infection and subsequent infertility is not fully understood.
Purpose of the Study:
- To investigate the genetic control of susceptibility to genital Chlamydia trachomatis infection.
- To compare the fertility and oviductal inflammation in different inbred mouse strains following genital infection.
- To determine if the H-2 major histocompatibility complex influences the outcome of Chlamydia trachomatis infection.
Main Methods:
- Genital infection of various inbred mouse strains (CBA, C3H, BALB/c, BALB/K) with a pathogenic human strain of Chlamydia trachomatis.
- Assessment of mouse fertility up to 6 months post-infection.
- Histological examination of oviductal inflammation (salpingitis) and development of hydrosalpinges.
Main Results:
- CBA, C3H (H-2o), and C3H/He-mg (H-2k) mice exhibited reduced fertility and significant oviductal inflammation post-infection.
- BALB/c (H-2d) and BALB/K (H-2k) mice showed no impairment in fertility and minimal oviductal inflammation.
- Susceptibility to salpingitis and infertility was genetically controlled, independent of the H-2 haplotype alone, as strains with the same H-2k haplotype showed different outcomes.
Conclusions:
- Host genetic factors play a crucial role in determining susceptibility to Chlamydia trachomatis-induced salpingitis and infertility.
- The H-2 major histocompatibility complex is not the sole determinant of resistance or susceptibility.
- Findings underscore the importance of early diagnosis and treatment of lower genital tract infections in women to prevent infertility.