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Updated: May 19, 2026

Mouse Models of Epididymitis Induced by Pathogen-Associated Molecular Patterns
Published on: December 12, 2025
Current methods and mechanisms for animal models of pelvic inflammatory disease: a review
1College of Traditional Chinese Medicine, Inner Mongolia Medical University, Hohhot, China.
Abstract:
Pelvic inflammatory disease (PID) is a complex multifactorial infectious disorder of the female reproductive tract, associated with severe long-term sequelae including infertility, ectopic pregnancy, and chronic pelvic pain, as well as elevated risks of endometriosis, cardiometabolic diseases, and colorectal cancer. Owing to ethical constraints on human research, animal models have become indispensable tools for investigating PID pathogenesis, evaluating therapeutic interventions, and developing novel diagnostic strategies. This review systematically summarizes current advances in PID animal model construction, with a focus on three core induction categories: pathogen, chemical, and physical induction methods. Pathogen induction utilizes single or multiple microorganisms (including Escherichia coli, Staphylococcus aureus, Chlamydia trachomatis, and Ureaplasma urealyticum) to recapitulate the infectious etiology of clinical PID. Chemical induction employs agents such as phenol mucilage, hydrochloric acid combined with lipopolysaccharide, and exogenous estrogen to simulate inflammatory processes via direct tissue damage or immune modulation. Physical induction methods include mechanical injury to disrupt mucosal barriers and foreign body implantation to mimic intrauterine device-related chronic inflammation. We further analyze integrated induction strategies that combine multiple approaches to improve model stability and pathological fidelity, and compare the strengths, limitations, and applicable scenarios of each modeling method. Finally, we discuss current gaps in PID animal model research, including the lack of standardized protocols, insufficient characterization of chronic disease progression, and limited translational relevance to human disease, and propose priorities for future model development to support preclinical research on PID prevention and treatment.

