The role of HLA-DR on plasmacytoid dendritic cells in mediating the effects of Butyrivibrio gut microbiota on Parkinson's disease.

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Title: The role of HLA-DR on plasmacytoid dendritic cells in mediating the effects of Butyrivibrio gut microbiota on Parkinson's disease.
Authors: Wang, Zihao (AUTHOR), Xia, Huan (AUTHOR), Feng, Tingting (AUTHOR), Aibibuli, Adilai (AUTHOR), Zhang, Mingyang (AUTHOR), Yang, Xinling (AUTHOR)
Source: Neurological Sciences. Aug2024, Vol. 45 Issue 8, p3809-3815. 7p.
Subjects: Gut microbiota, Parkinson's disease, Dendritic cells, HLA-DR antigens, Genome-wide association studies
Abstract: Background: Parkinson's disease (PD) is viewed as a progressively deteriorating neurodegenerative disorder, the exact etiology of which remains not fully deciphered to this date. The gut microbiota could play a crucial role in PD development by modulating the human immune system. Objective: This study aims to explore the relationship between gut microbiota and PD, focusing on how immune characteristics may both directly and indirectly influence their interaction. Methods: Utilizing cumulative data from genome-wide association studies (GWAS), our research conducted a two-sample Mendelian randomization (MR) analysis to clarify the association between the gut microbiome and PD. Additionally, by employing a two-step MR approach, we assessed the impact of gut microbiota on PD development via immune characteristics and quantified HLA-DR mediation effect on plasmacytoid dendritic cells (pDCs). Results: We discovered significant associations between PD and microbiota, comprising one class, one order, two families, and two genera. Furthermore, we explored the extent to which HLA-DR on pDCs mediates the effect of Butyrivibrio gut microbiota on PD. Conclusion: Our study emphasizes the complex interactions between the gut microbiota, immune characteristics, and PD. The relationships and intermediary roles identified in our research provide important insights for developing potential therapies that target the gut microbiome to alleviate symptoms in PD patients. [ABSTRACT FROM AUTHOR]
Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: The role of HLA-DR on plasmacytoid dendritic cells in mediating the effects of Butyrivibrio gut microbiota on Parkinson's disease.
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  Data: <searchLink fieldCode="AR" term="%22Wang%2C+Zihao%22">Wang, Zihao</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Xia%2C+Huan%22">Xia, Huan</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Feng%2C+Tingting%22">Feng, Tingting</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Aibibuli%2C+Adilai%22">Aibibuli, Adilai</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhang%2C+Mingyang%22">Zhang, Mingyang</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Yang%2C+Xinling%22">Yang, Xinling</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Neurological+Sciences%22">Neurological Sciences</searchLink>. Aug2024, Vol. 45 Issue 8, p3809-3815. 7p.
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  Data: <searchLink fieldCode="DE" term="%22Gut+microbiota%22">Gut microbiota</searchLink><br /><searchLink fieldCode="DE" term="%22Parkinson's+disease%22">Parkinson's disease</searchLink><br /><searchLink fieldCode="DE" term="%22Dendritic+cells%22">Dendritic cells</searchLink><br /><searchLink fieldCode="DE" term="%22HLA-DR+antigens%22">HLA-DR antigens</searchLink><br /><searchLink fieldCode="DE" term="%22Genome-wide+association+studies%22">Genome-wide association studies</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background: Parkinson's disease (PD) is viewed as a progressively deteriorating neurodegenerative disorder, the exact etiology of which remains not fully deciphered to this date. The gut microbiota could play a crucial role in PD development by modulating the human immune system. Objective: This study aims to explore the relationship between gut microbiota and PD, focusing on how immune characteristics may both directly and indirectly influence their interaction. Methods: Utilizing cumulative data from genome-wide association studies (GWAS), our research conducted a two-sample Mendelian randomization (MR) analysis to clarify the association between the gut microbiome and PD. Additionally, by employing a two-step MR approach, we assessed the impact of gut microbiota on PD development via immune characteristics and quantified HLA-DR mediation effect on plasmacytoid dendritic cells (pDCs). Results: We discovered significant associations between PD and microbiota, comprising one class, one order, two families, and two genera. Furthermore, we explored the extent to which HLA-DR on pDCs mediates the effect of Butyrivibrio gut microbiota on PD. Conclusion: Our study emphasizes the complex interactions between the gut microbiota, immune characteristics, and PD. The relationships and intermediary roles identified in our research provide important insights for developing potential therapies that target the gut microbiome to alleviate symptoms in PD patients. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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              Text: Aug2024
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