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Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model

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ABSTRACT

Pelvic inflammatory disease (PID), which is one of the most problematic complications experienced by women with sexually transmitted diseases, frequently causes secondary infections after reproductive abnormalities in veterinary animals. Although the uterus is self-protective, it becomes fragile during periods or pregnancy. To investigate PID, bacteria or lipopolysaccharide (LPS) extracted from gram negative bacteria has been used to induce the disease in several animal models. However, when LPS is applied to the peritoneum, it often causes systemic sepsis leading to death and the PID was not consistently demonstrated. Hydrochloric acid (HCl) has been used to induce inflammation in the lungs and stomach but not tested for reproductive organs. In this study, we developed a PID model in mice by HCl and LPS sequential intracervical (i.c.) administration. The proinflammatory cytokines, interleukin (IL)-1β, IL-6 and tumor necrosis factor-α, were detected in the mouse uterus by western blot analysis and cytokine enzyme-linked immunosorbent assay after HCl (25 mg/kg) administration i.c. followed by four LPS (50 mg/kg) treatments. Moreover, mice exhibited increased infiltration of neutrophils in the endometrium and epithelial layer. These results suggest that ic co-administration of HCl and LPS induces PID in mice. This new model may provide a consistent and reproducible PID model for future research.

No MeSH data available.


The representative histopathological findings of the uterus with saline only (A) and co-administration of HCl and LPS (B). (B) Mice were administered i.c. with HCl (25 mg/kg. 1 N) followed by four applications of LPS (50 mg/kg) every 2 h. Note the neutrophils in the lumen, in the endometrium and in the surface epithelial layer (arrows). No inflammation was observed in (A). L, lumen. H&E stain. 200×.
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Figure 4: The representative histopathological findings of the uterus with saline only (A) and co-administration of HCl and LPS (B). (B) Mice were administered i.c. with HCl (25 mg/kg. 1 N) followed by four applications of LPS (50 mg/kg) every 2 h. Note the neutrophils in the lumen, in the endometrium and in the surface epithelial layer (arrows). No inflammation was observed in (A). L, lumen. H&E stain. 200×.

Mentions: Uterine lesions in HCl-LPS50 (panel B in Fig. 4) and HCl-LPS25 (less intense; data not shown) were characterized by neutrophils infiltration, epithelial cell necrosis and degeneration, congestion and hemorrhage. In the other groups (LPS25ip, LPS50ip and HCl25), slight histopathological findings including congestion related edema and negligible infiltration of neutrophils were observed.


Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model
The representative histopathological findings of the uterus with saline only (A) and co-administration of HCl and LPS (B). (B) Mice were administered i.c. with HCl (25 mg/kg. 1 N) followed by four applications of LPS (50 mg/kg) every 2 h. Note the neutrophils in the lumen, in the endometrium and in the surface epithelial layer (arrows). No inflammation was observed in (A). L, lumen. H&E stain. 200×.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037311&req=5

Figure 4: The representative histopathological findings of the uterus with saline only (A) and co-administration of HCl and LPS (B). (B) Mice were administered i.c. with HCl (25 mg/kg. 1 N) followed by four applications of LPS (50 mg/kg) every 2 h. Note the neutrophils in the lumen, in the endometrium and in the surface epithelial layer (arrows). No inflammation was observed in (A). L, lumen. H&E stain. 200×.
Mentions: Uterine lesions in HCl-LPS50 (panel B in Fig. 4) and HCl-LPS25 (less intense; data not shown) were characterized by neutrophils infiltration, epithelial cell necrosis and degeneration, congestion and hemorrhage. In the other groups (LPS25ip, LPS50ip and HCl25), slight histopathological findings including congestion related edema and negligible infiltration of neutrophils were observed.

View Article: PubMed Central - PubMed

ABSTRACT

Pelvic inflammatory disease (PID), which is one of the most problematic complications experienced by women with sexually transmitted diseases, frequently causes secondary infections after reproductive abnormalities in veterinary animals. Although the uterus is self-protective, it becomes fragile during periods or pregnancy. To investigate PID, bacteria or lipopolysaccharide (LPS) extracted from gram negative bacteria has been used to induce the disease in several animal models. However, when LPS is applied to the peritoneum, it often causes systemic sepsis leading to death and the PID was not consistently demonstrated. Hydrochloric acid (HCl) has been used to induce inflammation in the lungs and stomach but not tested for reproductive organs. In this study, we developed a PID model in mice by HCl and LPS sequential intracervical (i.c.) administration. The proinflammatory cytokines, interleukin (IL)-1β, IL-6 and tumor necrosis factor-α, were detected in the mouse uterus by western blot analysis and cytokine enzyme-linked immunosorbent assay after HCl (25 mg/kg) administration i.c. followed by four LPS (50 mg/kg) treatments. Moreover, mice exhibited increased infiltration of neutrophils in the endometrium and epithelial layer. These results suggest that ic co-administration of HCl and LPS induces PID in mice. This new model may provide a consistent and reproducible PID model for future research.

No MeSH data available.