Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies
Patients with Parkinson’s disease (PD) exhibit distinct gut microbiota, which may promote gut-derived inflammation. Rifaximin is a nonabsorbable antibiotic that can modify gut microbiota. The present study investigated the effect of rifaximin on gut microbiota and inflammation status in PD. The stud...
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| Format: | Article |
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MDPI AG
2022-11-01
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| Online Access: | https://www.mdpi.com/2073-4409/11/21/3468 |
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| author | Chien-Tai Hong Lung Chan Kai-Yun Chen Hsun-Hua Lee Li-Kai Huang Yu-Chen S. H. Yang Yun-Ru Liu Chaur-Jong Hu |
| author_facet | Chien-Tai Hong Lung Chan Kai-Yun Chen Hsun-Hua Lee Li-Kai Huang Yu-Chen S. H. Yang Yun-Ru Liu Chaur-Jong Hu |
| author_sort | Chien-Tai Hong |
| collection | DOAJ |
| description | Patients with Parkinson’s disease (PD) exhibit distinct gut microbiota, which may promote gut-derived inflammation. Rifaximin is a nonabsorbable antibiotic that can modify gut microbiota. The present study investigated the effect of rifaximin on gut microbiota and inflammation status in PD. The study examined the effect of long-term rifaximin treatment on in vivo transgenic PD mice (MitoPark) and short-term rifaximin treatment on patients with PD. Rifaximin treatment caused a significant change in gut microbiota in the transgenic PD mice; in particular, it reduced the relative abundance of <i>Prevotellaceae UCG-001</i> and increased the relative abundance of <i>Bacteroides</i>, <i>Muribaculum</i>, and <i>Lachnospiraceae UCG-001</i>. Rifaximin treatment attenuated serum interleukin-1β, interleukin-6 and tumor necrosis factor-α, claudin-5 and occludin, which indicated the reduction of systemic inflammation and the protection of the blood–brain barrier integrity. The rifaximin-treated MitoPark mice exhibited better motor and memory performance than did the control mice, with lower microglial activation and increased neuronal survival in the hippocampus. In the patients with PD, 7-day rifaximin treatment caused an increase in the relative abundance of <i>Flavonifractor</i> 6 months after treatment, and the change in plasma proinflammatory cytokine levels was negatively associated with the baseline plasma interleukin-1α level. In conclusion, the present study demonstrated that rifaximin exerted a neuroprotective effect on the transgenic PD mice by modulating gut microbiota. We observed that patients with higher baseline inflammation possibly benefited from rifaximin treatment. With consideration for the tolerability and safety of rifaximin, randomized controlled trials should investigate the disease-modification effect of long-term treatment on select patients with PD. |
| first_indexed | 2024-03-09T19:11:31Z |
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| language | English |
| last_indexed | 2024-03-09T19:11:31Z |
| publishDate | 2022-11-01 |
| publisher | MDPI AG |
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| series | Cells |
| spelling | doaj.art-9c4c327bf9a347f196e7961010a4807f2023-11-24T04:09:16ZengMDPI AGCells2073-44092022-11-011121346810.3390/cells11213468Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical StudiesChien-Tai Hong0Lung Chan1Kai-Yun Chen2Hsun-Hua Lee3Li-Kai Huang4Yu-Chen S. H. Yang5Yun-Ru Liu6Chaur-Jong Hu7Department of Neurology, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, TaiwanDepartment of Neurology, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, TaiwanPh.D. Program in Medical Neuroscience, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, TaiwanDepartment of Neurology, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, TaiwanDepartment of Neurology, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, TaiwanJoint Biobank, Office of Human Research, Taipei Medical University, Taipei 11031, TaiwanJoint Biobank, Office of Human Research, Taipei Medical University, Taipei 11031, TaiwanDepartment of Neurology, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, TaiwanPatients with Parkinson’s disease (PD) exhibit distinct gut microbiota, which may promote gut-derived inflammation. Rifaximin is a nonabsorbable antibiotic that can modify gut microbiota. The present study investigated the effect of rifaximin on gut microbiota and inflammation status in PD. The study examined the effect of long-term rifaximin treatment on in vivo transgenic PD mice (MitoPark) and short-term rifaximin treatment on patients with PD. Rifaximin treatment caused a significant change in gut microbiota in the transgenic PD mice; in particular, it reduced the relative abundance of <i>Prevotellaceae UCG-001</i> and increased the relative abundance of <i>Bacteroides</i>, <i>Muribaculum</i>, and <i>Lachnospiraceae UCG-001</i>. Rifaximin treatment attenuated serum interleukin-1β, interleukin-6 and tumor necrosis factor-α, claudin-5 and occludin, which indicated the reduction of systemic inflammation and the protection of the blood–brain barrier integrity. The rifaximin-treated MitoPark mice exhibited better motor and memory performance than did the control mice, with lower microglial activation and increased neuronal survival in the hippocampus. In the patients with PD, 7-day rifaximin treatment caused an increase in the relative abundance of <i>Flavonifractor</i> 6 months after treatment, and the change in plasma proinflammatory cytokine levels was negatively associated with the baseline plasma interleukin-1α level. In conclusion, the present study demonstrated that rifaximin exerted a neuroprotective effect on the transgenic PD mice by modulating gut microbiota. We observed that patients with higher baseline inflammation possibly benefited from rifaximin treatment. With consideration for the tolerability and safety of rifaximin, randomized controlled trials should investigate the disease-modification effect of long-term treatment on select patients with PD.https://www.mdpi.com/2073-4409/11/21/3468rifaximingut microbiotaParkinson’s diseaseinflammation |
| spellingShingle | Chien-Tai Hong Lung Chan Kai-Yun Chen Hsun-Hua Lee Li-Kai Huang Yu-Chen S. H. Yang Yun-Ru Liu Chaur-Jong Hu Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies Cells rifaximin gut microbiota Parkinson’s disease inflammation |
| title | Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies |
| title_full | Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies |
| title_fullStr | Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies |
| title_full_unstemmed | Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies |
| title_short | Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies |
| title_sort | rifaximin modifies gut microbiota and attenuates inflammation in parkinson s disease preclinical and clinical studies |
| topic | rifaximin gut microbiota Parkinson’s disease inflammation |
| url | https://www.mdpi.com/2073-4409/11/21/3468 |
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