From mice to women and back again Causalities and clues for Chlamydia induced tubal ectopic pregnancy

Defining the molecular and cellular mechanisms of Chlamydia-induced tubal transport and progression of tubal implantation will be a key question for future studies.

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Authors

Ruijin Shao, M.D., Ph.D., Xiaoqin Wang, M.Sc., Wei Wang, M.D., Elisabet Stener-Victorin, R.P.T., Ph.D., Carina Mallard, Ph.D., Mats Brännström, M.D., Ph.D., Håkan Billig, M.D., Ph.D.

Vol 98, Issue 5, Pages 1175-1185

Abstract

Objective:

To provide an overview of knockout mouse models that have pathological tubal phenotypes after Chlamydia muridarum infection, discuss factors and pathological processes that contribute to inflammation, summarize data on tubal transport and progression of tubal implantation from studies in humans and animal models, and highlight research questions in the field.

Design:

A search of the relevant literature using PubMed and other online tools.

Setting:

University-based preclinical and clinical research laboratories.

Patients:

Women with tubal ectopic pregnancy following Chlamydia trachomatis infection.

Interventions:

None.

Main Outcome Measures:

Critical review of the literature.

Results:

Chlamydia trachomatis infection poses a major threat to human reproduction. Biological and epidemiological evidence suggests that progression of Chlamydia infection causes intense and persistent inflammation, injury, and scarring in the Fallopian tube, leading to substantially increased risk of ectopic pregnancy and infertility. The main targets of Chlamydia infection are epithelial cells lining the mucosal surface, which play a central role in host immune responses and pathophysiology. Tubal phenotypes at the cellular level in mutant mice appear to reflect alterations in the balance between inflammatory mediator and factor deficiency. While studies in mice infected with Chlamydia muridarum have provided insight into potential inflammatory mediators linked to Fallopian tube pathology, it is unclear how inflammation induced by Chlamydia infection prevents or retards normal tubal transport and causes embryo implantation in the Fallopian tube.

Conclusions:

Given the similarities in the tubal physiology of humans and rodents, knockout mouse models can be used to study certain aspects of tubal functions, such as gamete transport and early embryo implantation. Elucidation of the exact molecular mechanisms of immune and inflammatory responses caused by Chlamydia infection in human Fallopian tubal cells in vitro and understanding how Chlamydia infection affects tubal transport and implantation in animal studies in vivo may explain how Chlamydia trachomatis infection drives inflammation and develop the tubal pathology in women with tubal ectopic pregnancy.

Read the full text at: http://www.fertstert.org/article/S0015-0282(12)01849-3/fulltext


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Editorial Office, American Society for Reproductive Medicine

Fertility and Sterility® is an international journal for obstetricians, gynecologists, reproductive endocrinologists, urologists, basic scientists and others who treat and investigate problems of infertility and human reproductive disorders. The journal publishes juried original scientific articles in clinical and laboratory research relevant to reproductive endocrinology, urology, andrology, physiology, immunology, genetics, contraception, and menopause. Fertility and Sterility® encourages and supports meaningful basic and clinical research, and facilitates and promotes excellence in professional education, in the field of reproductive medicine.

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