Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammation
Long-term consumption of swainsonine could be poisonous to livestock, including facilitating apoptosis by impairing lysosomal function and inhibiting autophagic degradation, leading to liver inflammation and even death in livestock. However, the mechanism by swainsonine induced systemic inflammatory...
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| Language: | English |
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Elsevier
2024-10-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324009886 |
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| author | Ling Lei Dazhi Deng Wenqian Xu Mingyuan Yue Dandan Wu Keyi Fu Zunji Shi |
| author_facet | Ling Lei Dazhi Deng Wenqian Xu Mingyuan Yue Dandan Wu Keyi Fu Zunji Shi |
| author_sort | Ling Lei |
| collection | DOAJ |
| description | Long-term consumption of swainsonine could be poisonous to livestock, including facilitating apoptosis by impairing lysosomal function and inhibiting autophagic degradation, leading to liver inflammation and even death in livestock. However, the mechanism by swainsonine induced systemic inflammatory responses remained unclear, especially the effects of swainsonine on intestinal permeability, lipopolysaccharide (LPS) level and oxidative stress response were unknown. In this study, swainsonine increased intestinal permeability as evidenced by the significant down-regulation of colonic goblet cells, Akkermansia muciniphila and intestinal tight junction protein Occludin, Claudin 1 and ZO-1, and the significant up-regulation of mRNA expression level of the intestinal permeability indicator protein tyrosine phosphatase receptor type H (Ptprh) in the ileum of mice. Simultaneously, the elevated LPS biosynthetic genes in intestinal microbiota and increased intestinal permeability facilitated more bacterial endotoxin LPS to enter the blood. High concentration of free-form LPS induced high levels of proinflammatory cytokines and oxidative stress response, thereby causing the systemic inflammation. These findings provided a new perspective on swainsonine-induced systemic inflammation, suggesting that intestinal permeability and free-form LPS level may be the potential trigger factors. |
| format | Article |
| id | doaj-art-fd2ee42549a943d8ae78fedf4ddbfcb0 |
| institution | OA Journals |
| issn | 0147-6513 |
| language | English |
| publishDate | 2024-10-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-fd2ee42549a943d8ae78fedf4ddbfcb02025-08-20T01:54:44ZengElsevierEcotoxicology and Environmental Safety0147-65132024-10-0128411691210.1016/j.ecoenv.2024.116912Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammationLing Lei0Dazhi Deng1Wenqian Xu2Mingyuan Yue3Dandan Wu4Keyi Fu5Zunji Shi6Clinical Psychology, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Guangxi Key Laboratory of Reproductive Health and Birth Defect Prevention, Nanning, ChinaDepartment of Emergency, The People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Academy of Medical Sciences, Nanning 530021, ChinaState Key Laboratory of Herbage Improvement and Grassland Agro-ecosystems, Center for Grassland Microbiome, College of Pastoral Agriculture Science and Technology, Lanzhou University, Lanzhou 730000, ChinaState Key Laboratory of Herbage Improvement and Grassland Agro-ecosystems, Center for Grassland Microbiome, College of Pastoral Agriculture Science and Technology, Lanzhou University, Lanzhou 730000, ChinaState Key Laboratory of Herbage Improvement and Grassland Agro-ecosystems, Center for Grassland Microbiome, College of Pastoral Agriculture Science and Technology, Lanzhou University, Lanzhou 730000, ChinaState Key Laboratory of Herbage Improvement and Grassland Agro-ecosystems, Center for Grassland Microbiome, College of Pastoral Agriculture Science and Technology, Lanzhou University, Lanzhou 730000, China; Corresponding authors.State Key Laboratory of Herbage Improvement and Grassland Agro-ecosystems, Center for Grassland Microbiome, College of Pastoral Agriculture Science and Technology, Lanzhou University, Lanzhou 730000, China; Corresponding authors.Long-term consumption of swainsonine could be poisonous to livestock, including facilitating apoptosis by impairing lysosomal function and inhibiting autophagic degradation, leading to liver inflammation and even death in livestock. However, the mechanism by swainsonine induced systemic inflammatory responses remained unclear, especially the effects of swainsonine on intestinal permeability, lipopolysaccharide (LPS) level and oxidative stress response were unknown. In this study, swainsonine increased intestinal permeability as evidenced by the significant down-regulation of colonic goblet cells, Akkermansia muciniphila and intestinal tight junction protein Occludin, Claudin 1 and ZO-1, and the significant up-regulation of mRNA expression level of the intestinal permeability indicator protein tyrosine phosphatase receptor type H (Ptprh) in the ileum of mice. Simultaneously, the elevated LPS biosynthetic genes in intestinal microbiota and increased intestinal permeability facilitated more bacterial endotoxin LPS to enter the blood. High concentration of free-form LPS induced high levels of proinflammatory cytokines and oxidative stress response, thereby causing the systemic inflammation. These findings provided a new perspective on swainsonine-induced systemic inflammation, suggesting that intestinal permeability and free-form LPS level may be the potential trigger factors.http://www.sciencedirect.com/science/article/pii/S0147651324009886SwainsonineSystemic inflammationIntestinal permeabilityLipopolysaccharideOxidative stress |
| spellingShingle | Ling Lei Dazhi Deng Wenqian Xu Mingyuan Yue Dandan Wu Keyi Fu Zunji Shi Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammation Ecotoxicology and Environmental Safety Swainsonine Systemic inflammation Intestinal permeability Lipopolysaccharide Oxidative stress |
| title | Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammation |
| title_full | Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammation |
| title_fullStr | Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammation |
| title_full_unstemmed | Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammation |
| title_short | Increased intestinal permeability and lipopolysaccharide contribute to swainsonine-induced systemic inflammation |
| title_sort | increased intestinal permeability and lipopolysaccharide contribute to swainsonine induced systemic inflammation |
| topic | Swainsonine Systemic inflammation Intestinal permeability Lipopolysaccharide Oxidative stress |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324009886 |
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