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A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa
Septic arthritis is one of the most aggressive joint diseases. Although caused predominantly by S. aureus, Gram-negative bacteria, Pseudomonas aeruginosa among them, account for a significant percentage of the causal agents of septic arthritis. However, septic arthritis caused by P. aeruginosa has n...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856550/ https://www.ncbi.nlm.nih.gov/pubmed/31727989 http://dx.doi.org/10.1038/s41598-019-53434-5 |
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author | Jin, Tao Mohammad, Majd Hu, Zhicheng Fei, Ying Moore, Edward R. B. Pullerits, Rille Ali, Abukar |
author_facet | Jin, Tao Mohammad, Majd Hu, Zhicheng Fei, Ying Moore, Edward R. B. Pullerits, Rille Ali, Abukar |
author_sort | Jin, Tao |
collection | PubMed |
description | Septic arthritis is one of the most aggressive joint diseases. Although caused predominantly by S. aureus, Gram-negative bacteria, Pseudomonas aeruginosa among them, account for a significant percentage of the causal agents of septic arthritis. However, septic arthritis caused by P. aeruginosa has not been studied thus far, due to lack of an animal model. NMRI mice were inoculated with different doses of P. aeruginosa. The clinical course of septic arthritis and radiological changes of joints were examined. Furthermore, the host molecular and cellular mechanisms involved in P. aeruginosa-induced septic arthritis were investigated. Inoculation of mice with P. aeruginosa caused septic arthritis in a dose-dependent manner. Neutrophil depletion led to higher mortality and more severe joint destruction (p < 0.01). In contrast, monocyte depletion resulted in higher mortality (p < 0.05) but similar arthritis severity compared to controls. Mice depleted of CD4+ T-cells inoculated with P. aeruginosa displayed less severe bone damage (p < 0.05). For the first time, a mouse model for P. aeruginosa septic arthritis is presented. Our data demonstrate that neutrophils play a protective role in P. aeruginosa septic arthritis. Monocytes/macrophages, on the other hand, are only essential in preventing P. aeruginosa-induced mortality. Finally, CD4+ T-cells are pathogenic in P. aeruginosa septic arthritis. |
format | Online Article Text |
id | pubmed-6856550 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-68565502019-12-17 A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa Jin, Tao Mohammad, Majd Hu, Zhicheng Fei, Ying Moore, Edward R. B. Pullerits, Rille Ali, Abukar Sci Rep Article Septic arthritis is one of the most aggressive joint diseases. Although caused predominantly by S. aureus, Gram-negative bacteria, Pseudomonas aeruginosa among them, account for a significant percentage of the causal agents of septic arthritis. However, septic arthritis caused by P. aeruginosa has not been studied thus far, due to lack of an animal model. NMRI mice were inoculated with different doses of P. aeruginosa. The clinical course of septic arthritis and radiological changes of joints were examined. Furthermore, the host molecular and cellular mechanisms involved in P. aeruginosa-induced septic arthritis were investigated. Inoculation of mice with P. aeruginosa caused septic arthritis in a dose-dependent manner. Neutrophil depletion led to higher mortality and more severe joint destruction (p < 0.01). In contrast, monocyte depletion resulted in higher mortality (p < 0.05) but similar arthritis severity compared to controls. Mice depleted of CD4+ T-cells inoculated with P. aeruginosa displayed less severe bone damage (p < 0.05). For the first time, a mouse model for P. aeruginosa septic arthritis is presented. Our data demonstrate that neutrophils play a protective role in P. aeruginosa septic arthritis. Monocytes/macrophages, on the other hand, are only essential in preventing P. aeruginosa-induced mortality. Finally, CD4+ T-cells are pathogenic in P. aeruginosa septic arthritis. Nature Publishing Group UK 2019-11-14 /pmc/articles/PMC6856550/ /pubmed/31727989 http://dx.doi.org/10.1038/s41598-019-53434-5 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Jin, Tao Mohammad, Majd Hu, Zhicheng Fei, Ying Moore, Edward R. B. Pullerits, Rille Ali, Abukar A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa |
title | A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa |
title_full | A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa |
title_fullStr | A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa |
title_full_unstemmed | A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa |
title_short | A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa |
title_sort | novel mouse model for septic arthritis induced by pseudomonas aeruginosa |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856550/ https://www.ncbi.nlm.nih.gov/pubmed/31727989 http://dx.doi.org/10.1038/s41598-019-53434-5 |
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