Gut microbiota exaggerates triclosan-induced liver injury via gut-liver axis
Triclosan (TCS) is an antimicrobial ingredient that has been widely incorporated in consumer products. TCS can cause hepatic damage by disturbing lipid metabolism, which is often accompanied with gut microbiota dysbiosis. However, the effects of gut microbiota on the TCS-induced liver injury are sti...
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| Published in | Journal of hazardous materials Vol. 421; p. 126707 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Elsevier B.V
05.01.2022
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Triclosan (TCS) is an antimicrobial ingredient that has been widely incorporated in consumer products. TCS can cause hepatic damage by disturbing lipid metabolism, which is often accompanied with gut microbiota dysbiosis. However, the effects of gut microbiota on the TCS-induced liver injury are still unknown. Therefore, we constructed a mouse model based on five-week-old male C57BL/6 mice to investigate the effects of dietary TCS exposure (40 ppm) on liver injury. We found that TCS treatment for 4 weeks dramatically disturbed gut microbiota homeostasis, resulting in overproduction of lipopolysaccharides (LPS) and deficiency of secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid (LCA). In addition, TCS considerably increased intestinal permeability by reducing mucus excretion and expression of tight junction proteins (ZO-1, occludin and claudin 4), which facilitated translocation of LPS. The LPS accumulation in blood contributed to liver injury by triggering the inflammatory response via TLR4 pathway. In summary, this study provides novel insights into the underlying mechanisms of TCS–associated liver injury induced by gut microbiota via the gut–liver axis, and contributes to better interpretation of the health impact of the environmentally emerging contaminant TCS.
[Display omitted]
•TCS perturbed the gut microbiota in mice and increased its pathogenic potential.•TCS induced gut leaky via downregulating the expression of tight junction proteins.•TCS promoted liver inflammation via the TLR4 pathway and TGR5 pathway in mice.•Mechanism of gut-liver axis provided novel insight into the underlying TCS toxicity. |
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| AbstractList | Triclosan (TCS) is an antimicrobial ingredient that has been widely incorporated in consumer products. TCS can cause hepatic damage by disturbing lipid metabolism, which is often accompanied with gut microbiota dysbiosis. However, the effects of gut microbiota on the TCS-induced liver injury are still unknown. Therefore, we constructed a mouse model based on five-week-old male C57BL/6 mice to investigate the effects of dietary TCS exposure (40 ppm) on liver injury. We found that TCS treatment for 4 weeks dramatically disturbed gut microbiota homeostasis, resulting in overproduction of lipopolysaccharides (LPS) and deficiency of secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid (LCA). In addition, TCS considerably increased intestinal permeability by reducing mucus excretion and expression of tight junction proteins (ZO-1, occludin and claudin 4), which facilitated translocation of LPS. The LPS accumulation in blood contributed to liver injury by triggering the inflammatory response via TLR4 pathway. In summary, this study provides novel insights into the underlying mechanisms of TCS–associated liver injury induced by gut microbiota via the gut–liver axis, and contributes to better interpretation of the health impact of the environmentally emerging contaminant TCS. Triclosan (TCS) is an antimicrobial ingredient that has been widely incorporated in consumer products. TCS can cause hepatic damage by disturbing lipid metabolism, which is often accompanied with gut microbiota dysbiosis. However, the effects of gut microbiota on the TCS-induced liver injury are still unknown. Therefore, we constructed a mouse model based on five-week-old male C57BL/6 mice to investigate the effects of dietary TCS exposure (40 ppm) on liver injury. We found that TCS treatment for 4 weeks dramatically disturbed gut microbiota homeostasis, resulting in overproduction of lipopolysaccharides (LPS) and deficiency of secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid (LCA). In addition, TCS considerably increased intestinal permeability by reducing mucus excretion and expression of tight junction proteins (ZO-1, occludin and claudin 4), which facilitated translocation of LPS. The LPS accumulation in blood contributed to liver injury by triggering the inflammatory response via TLR4 pathway. In summary, this study provides novel insights into the underlying mechanisms of TCS-associated liver injury induced by gut microbiota via the gut-liver axis, and contributes to better interpretation of the health impact of the environmentally emerging contaminant TCS.Triclosan (TCS) is an antimicrobial ingredient that has been widely incorporated in consumer products. TCS can cause hepatic damage by disturbing lipid metabolism, which is often accompanied with gut microbiota dysbiosis. However, the effects of gut microbiota on the TCS-induced liver injury are still unknown. Therefore, we constructed a mouse model based on five-week-old male C57BL/6 mice to investigate the effects of dietary TCS exposure (40 ppm) on liver injury. We found that TCS treatment for 4 weeks dramatically disturbed gut microbiota homeostasis, resulting in overproduction of lipopolysaccharides (LPS) and deficiency of secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid (LCA). In addition, TCS considerably increased intestinal permeability by reducing mucus excretion and expression of tight junction proteins (ZO-1, occludin and claudin 4), which facilitated translocation of LPS. The LPS accumulation in blood contributed to liver injury by triggering the inflammatory response via TLR4 pathway. In summary, this study provides novel insights into the underlying mechanisms of TCS-associated liver injury induced by gut microbiota via the gut-liver axis, and contributes to better interpretation of the health impact of the environmentally emerging contaminant TCS. Triclosan (TCS) is an antimicrobial ingredient that has been widely incorporated in consumer products. TCS can cause hepatic damage by disturbing lipid metabolism, which is often accompanied with gut microbiota dysbiosis. However, the effects of gut microbiota on the TCS-induced liver injury are still unknown. Therefore, we constructed a mouse model based on five-week-old male C57BL/6 mice to investigate the effects of dietary TCS exposure (40 ppm) on liver injury. We found that TCS treatment for 4 weeks dramatically disturbed gut microbiota homeostasis, resulting in overproduction of lipopolysaccharides (LPS) and deficiency of secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid (LCA). In addition, TCS considerably increased intestinal permeability by reducing mucus excretion and expression of tight junction proteins (ZO-1, occludin and claudin 4), which facilitated translocation of LPS. The LPS accumulation in blood contributed to liver injury by triggering the inflammatory response via TLR4 pathway. In summary, this study provides novel insights into the underlying mechanisms of TCS–associated liver injury induced by gut microbiota via the gut–liver axis, and contributes to better interpretation of the health impact of the environmentally emerging contaminant TCS. [Display omitted] •TCS perturbed the gut microbiota in mice and increased its pathogenic potential.•TCS induced gut leaky via downregulating the expression of tight junction proteins.•TCS promoted liver inflammation via the TLR4 pathway and TGR5 pathway in mice.•Mechanism of gut-liver axis provided novel insight into the underlying TCS toxicity. |
| ArticleNumber | 126707 |
| Author | Zhang, Peng Duan, Yitao Mao, Daqing Zheng, Liyang Luo, Yi Gao, Yuting Gao, Huihui |
| Author_xml | – sequence: 1 givenname: Peng surname: Zhang fullname: Zhang, Peng organization: College of Environmental Sciences and Engineering, Nankai University, Tianjin 300350, China – sequence: 2 givenname: Liyang surname: Zheng fullname: Zheng, Liyang organization: School of Medicine, Nankai University, Tianjin 300071, China – sequence: 3 givenname: Yitao surname: Duan fullname: Duan, Yitao organization: College of Environmental Sciences and Engineering, Nankai University, Tianjin 300350, China – sequence: 4 givenname: Yuting surname: Gao fullname: Gao, Yuting organization: College of Environmental Sciences and Engineering, Nankai University, Tianjin 300350, China – sequence: 5 givenname: Huihui surname: Gao fullname: Gao, Huihui organization: School of Medicine, Nankai University, Tianjin 300071, China – sequence: 6 givenname: Daqing surname: Mao fullname: Mao, Daqing email: maodq@nankai.edu.cn organization: School of Medicine, Nankai University, Tianjin 300071, China – sequence: 7 givenname: Yi surname: Luo fullname: Luo, Yi email: luoy@nankai.edu.cn organization: College of Environmental Sciences and Engineering, Nankai University, Tianjin 300350, China |
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| Snippet | Triclosan (TCS) is an antimicrobial ingredient that has been widely incorporated in consumer products. TCS can cause hepatic damage by disturbing lipid... |
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| SubjectTerms | bile blood deoxycholic acid dysbiosis excretion Gut microbiota Gut–liver axis homeostasis inflammation Inflammatory responses ingredients intestinal microorganisms intestines lipid metabolism Lipopolysaccharide lipopolysaccharides lithocholic acid liver Liver injury males mice mucus occludins permeability tight junctions TLR4 Triclosan |
| Title | Gut microbiota exaggerates triclosan-induced liver injury via gut-liver axis |
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