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Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model
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 dur...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Veterinary Science
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037311/ https://www.ncbi.nlm.nih.gov/pubmed/26726020 http://dx.doi.org/10.4142/jvs.2016.17.3.413 |
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author | Oh, Yeonsu Lee, Jaehun Kim, Hyeon-Cheol Hahn, Tae-Wook Yoon, Byung-Il Han, Jeong-Hee Kwon, Yong-Soo Park, Joung Jun Koo, Deog-Bon Rhee, Ki-Jong Jung, Bae Dong |
author_facet | Oh, Yeonsu Lee, Jaehun Kim, Hyeon-Cheol Hahn, Tae-Wook Yoon, Byung-Il Han, Jeong-Hee Kwon, Yong-Soo Park, Joung Jun Koo, Deog-Bon Rhee, Ki-Jong Jung, Bae Dong |
author_sort | Oh, Yeonsu |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5037311 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The Korean Society of Veterinary Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-50373112016-09-29 Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model Oh, Yeonsu Lee, Jaehun Kim, Hyeon-Cheol Hahn, Tae-Wook Yoon, Byung-Il Han, Jeong-Hee Kwon, Yong-Soo Park, Joung Jun Koo, Deog-Bon Rhee, Ki-Jong Jung, Bae Dong J Vet Sci Original Article 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. The Korean Society of Veterinary Science 2016-09 2016-09-20 /pmc/articles/PMC5037311/ /pubmed/26726020 http://dx.doi.org/10.4142/jvs.2016.17.3.413 Text en © 2016 The Korean Society of Veterinary Science. http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Oh, Yeonsu Lee, Jaehun Kim, Hyeon-Cheol Hahn, Tae-Wook Yoon, Byung-Il Han, Jeong-Hee Kwon, Yong-Soo Park, Joung Jun Koo, Deog-Bon Rhee, Ki-Jong Jung, Bae Dong Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model |
title | Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model |
title_full | Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model |
title_fullStr | Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model |
title_full_unstemmed | Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model |
title_short | Establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model |
title_sort | establishment of hydrochloric acid/lipopolysaccharide-induced pelvic inflammatory disease model |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037311/ https://www.ncbi.nlm.nih.gov/pubmed/26726020 http://dx.doi.org/10.4142/jvs.2016.17.3.413 |
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