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Retinitis pigmentosa is associated with shifts in the gut microbiome

The gut microbiome is known to influence the pathogenesis and progression of neurodegenerative diseases. However, there has been relatively little focus upon the implications of the gut microbiome in retinal diseases such as retinitis pigmentosa (RP). Here, we investigated changes in gut microbiome...

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Autores principales: Kutsyr, Oksana, Maestre-Carballa, Lucía, Lluesma-Gomez, Mónica, Martinez-Garcia, Manuel, Cuenca, Nicolás, Lax, Pedro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7988170/
https://www.ncbi.nlm.nih.gov/pubmed/33758301
http://dx.doi.org/10.1038/s41598-021-86052-1
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author Kutsyr, Oksana
Maestre-Carballa, Lucía
Lluesma-Gomez, Mónica
Martinez-Garcia, Manuel
Cuenca, Nicolás
Lax, Pedro
author_facet Kutsyr, Oksana
Maestre-Carballa, Lucía
Lluesma-Gomez, Mónica
Martinez-Garcia, Manuel
Cuenca, Nicolás
Lax, Pedro
author_sort Kutsyr, Oksana
collection PubMed
description The gut microbiome is known to influence the pathogenesis and progression of neurodegenerative diseases. However, there has been relatively little focus upon the implications of the gut microbiome in retinal diseases such as retinitis pigmentosa (RP). Here, we investigated changes in gut microbiome composition linked to RP, by assessing both retinal degeneration and gut microbiome in the rd10 mouse model of RP as compared to control C57BL/6J mice. In rd10 mice, retinal responsiveness to flashlight stimuli and visual acuity were deteriorated with respect to observed in age-matched control mice. This functional decline in dystrophic animals was accompanied by photoreceptor loss, morphologic anomalies in photoreceptor cells and retinal reactive gliosis. Furthermore, 16S rRNA gene amplicon sequencing data showed a microbial gut dysbiosis with differences in alpha and beta diversity at the genera, species and amplicon sequence variants (ASV) levels between dystrophic and control mice. Remarkably, four fairly common ASV in healthy gut microbiome belonging to Rikenella spp., Muribaculaceace spp., Prevotellaceae UCG-001 spp., and Bacilli spp. were absent in the gut microbiome of retinal disease mice, while Bacteroides caecimuris was significantly enriched in mice with RP. The results indicate that retinal degenerative changes in RP are linked to relevant gut microbiome changes. The findings suggest that microbiome shifting could be considered as potential biomarker and therapeutic target for retinal degenerative diseases.
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spelling pubmed-79881702021-03-26 Retinitis pigmentosa is associated with shifts in the gut microbiome Kutsyr, Oksana Maestre-Carballa, Lucía Lluesma-Gomez, Mónica Martinez-Garcia, Manuel Cuenca, Nicolás Lax, Pedro Sci Rep Article The gut microbiome is known to influence the pathogenesis and progression of neurodegenerative diseases. However, there has been relatively little focus upon the implications of the gut microbiome in retinal diseases such as retinitis pigmentosa (RP). Here, we investigated changes in gut microbiome composition linked to RP, by assessing both retinal degeneration and gut microbiome in the rd10 mouse model of RP as compared to control C57BL/6J mice. In rd10 mice, retinal responsiveness to flashlight stimuli and visual acuity were deteriorated with respect to observed in age-matched control mice. This functional decline in dystrophic animals was accompanied by photoreceptor loss, morphologic anomalies in photoreceptor cells and retinal reactive gliosis. Furthermore, 16S rRNA gene amplicon sequencing data showed a microbial gut dysbiosis with differences in alpha and beta diversity at the genera, species and amplicon sequence variants (ASV) levels between dystrophic and control mice. Remarkably, four fairly common ASV in healthy gut microbiome belonging to Rikenella spp., Muribaculaceace spp., Prevotellaceae UCG-001 spp., and Bacilli spp. were absent in the gut microbiome of retinal disease mice, while Bacteroides caecimuris was significantly enriched in mice with RP. The results indicate that retinal degenerative changes in RP are linked to relevant gut microbiome changes. The findings suggest that microbiome shifting could be considered as potential biomarker and therapeutic target for retinal degenerative diseases. Nature Publishing Group UK 2021-03-23 /pmc/articles/PMC7988170/ /pubmed/33758301 http://dx.doi.org/10.1038/s41598-021-86052-1 Text en © The Author(s) 2021 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Kutsyr, Oksana
Maestre-Carballa, Lucía
Lluesma-Gomez, Mónica
Martinez-Garcia, Manuel
Cuenca, Nicolás
Lax, Pedro
Retinitis pigmentosa is associated with shifts in the gut microbiome
title Retinitis pigmentosa is associated with shifts in the gut microbiome
title_full Retinitis pigmentosa is associated with shifts in the gut microbiome
title_fullStr Retinitis pigmentosa is associated with shifts in the gut microbiome
title_full_unstemmed Retinitis pigmentosa is associated with shifts in the gut microbiome
title_short Retinitis pigmentosa is associated with shifts in the gut microbiome
title_sort retinitis pigmentosa is associated with shifts in the gut microbiome
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7988170/
https://www.ncbi.nlm.nih.gov/pubmed/33758301
http://dx.doi.org/10.1038/s41598-021-86052-1
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