From mice to women and back again: causalities and clues for Chlamydia-induced tubal ectopic pregnancy.

摘要: Objective To provide an overview of knockout mouse models that have pathological tubal phenotypes after Chlamydia muridarum infection, discuss factors and processes contribute to inflammation, summarize data on transport progression implantation from studies in humans animal models, highlight research questions the field. Design A search relevant literature using PubMed other online tools. Setting University-based preclinical clinical laboratories. Patient(s) Women with ectopic pregnancy trachomatis infection. Intervention(s) None. Main Outcome Measure(s) Critical review literature. Result(s) infection poses a major threat human reproduction. Biological epidemiological evidence suggests causes intense persistent injury, scarring fallopian tube, leading substantially increased risk infertility. The main targets are epithelial cells lining mucosal surface, which play central role host immune responses pathophysiology. Tubal at cellular level mutant mice appear reflect alterations balance between inflammatory mediator factor deficiency. While infected provided insight into potential mediators linked tube pathology, it is unclear how inflammation induced by prevents or retards normal embryo tube. Conclusion(s) Given similarities physiology rodents, can be used study certain aspects functions, such as gamete early implantation. Elucidation exact molecular mechanisms caused in vitro understanding affects in vivo may explain drives develops pathology women pregnancy.