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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 the number of infiltrated neutrophils per unit area (0.25 mm2) in uterine tissue of different experimental groups. *Significantly increased number of neutrophils in LPS25 and LPS50 groups than in LPS25ip, LPS50ip, and Negative control groups (p < 0.05). ***Significantly increased number of neutrophils in HCl-LPS25 and HCl-LPS 50 groups compared with other groups (p < 0.001).
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Figure 6: Bar graphs for the number of infiltrated neutrophils per unit area (0.25 mm2) in uterine tissue of different experimental groups. *Significantly increased number of neutrophils in LPS25 and LPS50 groups than in LPS25ip, LPS50ip, and Negative control groups (p < 0.05). ***Significantly increased number of neutrophils in HCl-LPS25 and HCl-LPS 50 groups compared with other groups (p < 0.001).

Mentions: The scores of uterine lesions and numbers of infiltrated neutrophils were significantly higher in the combined treated HCl-LPS50 and HCl-LPS25 groups (p < 0.001) than other groups, followed by single treated LPS50ic and LPS25ic groups (p < 0.05) and then the remaining groups (Figs. 5 and 6). The number of infiltrated neutrophils was correlated with pro-inflammatory cytokine expression in uterine tissue (TNF-α, r = 0.853, p < 0.001; IL-1β, r = 0.798, p < 0.001; IL-6, r = 0.785, p < 0.001) and histopathological scores (r = 0.669, p < 0.001), but not correlated with clinical sign scores (r = 0.293, p = 0.069).


Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model
Bar graphs for the number of infiltrated neutrophils per unit area (0.25 mm2) in uterine tissue of different experimental groups. *Significantly increased number of neutrophils in LPS25 and LPS50 groups than in LPS25ip, LPS50ip, and Negative control groups (p < 0.05). ***Significantly increased number of neutrophils in HCl-LPS25 and HCl-LPS 50 groups compared with other groups (p < 0.001).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 6: Bar graphs for the number of infiltrated neutrophils per unit area (0.25 mm2) in uterine tissue of different experimental groups. *Significantly increased number of neutrophils in LPS25 and LPS50 groups than in LPS25ip, LPS50ip, and Negative control groups (p < 0.05). ***Significantly increased number of neutrophils in HCl-LPS25 and HCl-LPS 50 groups compared with other groups (p < 0.001).
Mentions: The scores of uterine lesions and numbers of infiltrated neutrophils were significantly higher in the combined treated HCl-LPS50 and HCl-LPS25 groups (p < 0.001) than other groups, followed by single treated LPS50ic and LPS25ic groups (p < 0.05) and then the remaining groups (Figs. 5 and 6). The number of infiltrated neutrophils was correlated with pro-inflammatory cytokine expression in uterine tissue (TNF-α, r = 0.853, p < 0.001; IL-1β, r = 0.798, p < 0.001; IL-6, r = 0.785, p < 0.001) and histopathological scores (r = 0.669, p < 0.001), but not correlated with clinical sign scores (r = 0.293, p = 0.069).

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.