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

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.


Changes in cytokine expression in uterine tissue after co-administration of HCl and LPS. (A) Mice were administered i.c. with HCl (25 mg/kg) followed by four applications of LPS (25 mg/kg or 50 mg/kg) every 2 h. Two hours after the final injection, the uterus was removed and protein expression was assessed by Western blot. (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.
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Figure 2: Changes in cytokine expression in uterine tissue after co-administration of HCl and LPS. (A) Mice were administered i.c. with HCl (25 mg/kg) followed by four applications of LPS (25 mg/kg or 50 mg/kg) every 2 h. Two hours after the final injection, the uterus was removed and protein expression was assessed by Western blot. (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.

Mentions: To investigate the inflammatory cytokine expression levels, IL-1β, IL-6, and TNF-α were evaluated in inflammation induced uterine tissues. Western blot analysis revealed that no cytokines were present in the uterine tissues from any of the single agent treated groups with various administration schemes, including LPS25ip, LPS50ip, LPS25ic, LPS50ic, and HCl25 and one combined treatment group, HCl-LPS25 (data not shown). Additionally, all tested cytokines were detected only in the HCl-LPS50 combined treatment group (Fig. 2).


Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model
Changes in cytokine expression in uterine tissue after co-administration of HCl and LPS. (A) Mice were administered i.c. with HCl (25 mg/kg) followed by four applications of LPS (25 mg/kg or 50 mg/kg) every 2 h. Two hours after the final injection, the uterus was removed and protein expression was assessed by Western blot. (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.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Changes in cytokine expression in uterine tissue after co-administration of HCl and LPS. (A) Mice were administered i.c. with HCl (25 mg/kg) followed by four applications of LPS (25 mg/kg or 50 mg/kg) every 2 h. Two hours after the final injection, the uterus was removed and protein expression was assessed by Western blot. (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.
Mentions: To investigate the inflammatory cytokine expression levels, IL-1β, IL-6, and TNF-α were evaluated in inflammation induced uterine tissues. Western blot analysis revealed that no cytokines were present in the uterine tissues from any of the single agent treated groups with various administration schemes, including LPS25ip, LPS50ip, LPS25ic, LPS50ic, and HCl25 and one combined treatment group, HCl-LPS25 (data not shown). Additionally, all tested cytokines were detected only in the HCl-LPS50 combined treatment group (Fig. 2).

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.