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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.


Bar graphs for inflammatory cytokines measured by enzyme-linked immunosorbent assay in the uterine tissues of different experimental groups and a normal control. *Significantly higher inflammatory cytokine levels than the HCl25 and Neg CTL groups (p < 0.05). ***Significantly higher inflammatory cytokine levels in the uteruses of HCl-LPS combined with i.c. administered animals (p < 0.001).
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Figure 3: Bar graphs for inflammatory cytokines measured by enzyme-linked immunosorbent assay in the uterine tissues of different experimental groups and a normal control. *Significantly higher inflammatory cytokine levels than the HCl25 and Neg CTL groups (p < 0.05). ***Significantly higher inflammatory cytokine levels in the uteruses of HCl-LPS combined with i.c. administered animals (p < 0.001).

Mentions: HCl-LPS combined treatment induced significantly higher levels of IL-1β, IL-6 and TNF-α in uteruses (p < 0.001). In other groups, IL-1β and IL-6 levels were detected in trace amounts, but no significant differences were observed, rather, the TNF-α level was significantly upregulated in LPS25ip, LPS50ip, LPS25ic, and LPS50ic treated groups (p < 0.05; Fig. 3).


Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model
Bar graphs for inflammatory cytokines measured by enzyme-linked immunosorbent assay in the uterine tissues of different experimental groups and a normal control. *Significantly higher inflammatory cytokine levels than the HCl25 and Neg CTL groups (p < 0.05). ***Significantly higher inflammatory cytokine levels in the uteruses of HCl-LPS combined with i.c. administered animals (p < 0.001).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Bar graphs for inflammatory cytokines measured by enzyme-linked immunosorbent assay in the uterine tissues of different experimental groups and a normal control. *Significantly higher inflammatory cytokine levels than the HCl25 and Neg CTL groups (p < 0.05). ***Significantly higher inflammatory cytokine levels in the uteruses of HCl-LPS combined with i.c. administered animals (p < 0.001).
Mentions: HCl-LPS combined treatment induced significantly higher levels of IL-1β, IL-6 and TNF-α in uteruses (p < 0.001). In other groups, IL-1β and IL-6 levels were detected in trace amounts, but no significant differences were observed, rather, the TNF-α level was significantly upregulated in LPS25ip, LPS50ip, LPS25ic, and LPS50ic treated groups (p < 0.05; Fig. 3).

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)-1&beta;, IL-6 and tumor necrosis factor-&alpha;, 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.