Identifying the clinical presentations, progression, and sequela of pelvic inflammatory disease through physiological, histological and ultrastructural evaluation of a rat animal model

Patients with pelvic inflammatory disease (PID) are at an increased risk of ectopic pregnancy, infertility, and varying degrees of chronic pelvic pain. The aims of this study were to establish a rat model of PID and characterize its progression in order to assist in the study of pathophysiological mechanisms and to provide animal model for future studies of PID treatments.

This study clearly described the characteristics and progression of PID in a rat model. The detailed evidence increased our understanding of the pathogenesis and progression of PID and may be useful for future studies of PID treatments.

Fifty Sprague-Dawley rats (female, 6-weeks-old) were divided into a model group (n=28) and a control group (n=22). The rat endometrium was mechanically injured by a needle which moved back and forth 3 times on the endometrial tissue, and a mixed bacterial solution (6×108 CFU) of equal concentrations of Escherichia coli and Staphylococcus aureus was injected into both horns of the rat uterus. Physiological characteristics including weight, temperature, blood, and inflammatory factors were compared, and immunohistochemistry and transmission electron microscopy were used to evaluate the progress and sequela of PID.

The model rats experienced acute PID in the first 14 days and exhibited higher body temperatures and decreased body weight. Infection-related factors in the blood were also significantly changed compared with the normal group, with obviously increased serum levels of C-reactive protein (CRP), interferon gamma (IFN-γ), and interleukin-4 (IL-4). Congestion and edema were observed in the uteri of the model rats, followed by infiltration of numerous inflammatory cells and ultrastructural morphology changes. Histological examination of the uterus showed that adhesion initially appeared at approximately 21 days. In addition to the increased collagen fibers biomass, the expression of transforming growth factor-beta 1 (TGF-β1) was elevated, which might have contributed to pelvic tissue adhesion formation in the PID sequela. Conclusions: This study clearly described the characteristics and progression of PID in a rat model. The detailed evidence increased our understanding of the pathogenesis and progression of PID and may be useful for future studies of PID treatments.