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Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes

BACKGROUND: Hypertension is associated with gut dysbiosis, altered intestinal immunity, and gut pathology in animal models and humans. Although these findings have implicated impaired interactions between gut and gut microbiota in hypertension, little is known about the specific functional gut micro...

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Autores principales: Li, Jing, Richards, Elaine M., Tummala, Ramakumar, Pepine, Carl J., Raizada, Mohan K., Yang, Tao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10111478/
https://www.ncbi.nlm.nih.gov/pubmed/36752270
http://dx.doi.org/10.1161/JAHA.122.027918
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author Li, Jing
Richards, Elaine M.
Tummala, Ramakumar
Pepine, Carl J.
Raizada, Mohan K.
Yang, Tao
author_facet Li, Jing
Richards, Elaine M.
Tummala, Ramakumar
Pepine, Carl J.
Raizada, Mohan K.
Yang, Tao
author_sort Li, Jing
collection PubMed
description BACKGROUND: Hypertension is associated with gut dysbiosis, altered intestinal immunity, and gut pathology in animal models and humans. Although these findings have implicated impaired interactions between gut and gut microbiota in hypertension, little is known about the specific functional gut microbes that interact with intestinal mucosa. METHODS AND RESULTS: To identify these microbes, we sorted Immunoglobin A (IgA)‐coated (IgA(+)) and IgA‐noncoated (IgA(−)) bacteria using a combination of magnetic‐activated cell sorting and fluorescence‐activated cell sorting, and subsequently performed 16 S rRNA gene sequencing (IgA‐SEQ) to determine the microbial composition of IgA(+) and IgA(−) fractions in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats. We observed a significant decrease in IgA(+) bacteria in SHR compared with Wistar Kyoto and a distinct composition of IgA(+) and IgA(−) bacteria between Wistar Kyoto and SHR, showing more IgA‐bound Proteobacteria, Bacteroidetes and Actinobacteria but less of Firmicutes in SHR at the phylum level. We further identified enriched IgA‐coated Romboutsia, Turicibacter, Ileibacterium, and Dubosiella in SHR that were negatively correlated with the various pathways including antigen presentation, immune response, cell junction organization, epithelium development, and defense response to virus. CONCLUSIONS: We demonstrate new IgA‐coated bacteria that participate in host‐microbiota communication in hypertension, suggesting promising therapeutic interventions targeting these bacteria for hypertension management.
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spelling pubmed-101114782023-04-19 Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes Li, Jing Richards, Elaine M. Tummala, Ramakumar Pepine, Carl J. Raizada, Mohan K. Yang, Tao J Am Heart Assoc Brief Communication BACKGROUND: Hypertension is associated with gut dysbiosis, altered intestinal immunity, and gut pathology in animal models and humans. Although these findings have implicated impaired interactions between gut and gut microbiota in hypertension, little is known about the specific functional gut microbes that interact with intestinal mucosa. METHODS AND RESULTS: To identify these microbes, we sorted Immunoglobin A (IgA)‐coated (IgA(+)) and IgA‐noncoated (IgA(−)) bacteria using a combination of magnetic‐activated cell sorting and fluorescence‐activated cell sorting, and subsequently performed 16 S rRNA gene sequencing (IgA‐SEQ) to determine the microbial composition of IgA(+) and IgA(−) fractions in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats. We observed a significant decrease in IgA(+) bacteria in SHR compared with Wistar Kyoto and a distinct composition of IgA(+) and IgA(−) bacteria between Wistar Kyoto and SHR, showing more IgA‐bound Proteobacteria, Bacteroidetes and Actinobacteria but less of Firmicutes in SHR at the phylum level. We further identified enriched IgA‐coated Romboutsia, Turicibacter, Ileibacterium, and Dubosiella in SHR that were negatively correlated with the various pathways including antigen presentation, immune response, cell junction organization, epithelium development, and defense response to virus. CONCLUSIONS: We demonstrate new IgA‐coated bacteria that participate in host‐microbiota communication in hypertension, suggesting promising therapeutic interventions targeting these bacteria for hypertension management. John Wiley and Sons Inc. 2023-02-08 /pmc/articles/PMC10111478/ /pubmed/36752270 http://dx.doi.org/10.1161/JAHA.122.027918 Text en © 2023 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Brief Communication
Li, Jing
Richards, Elaine M.
Tummala, Ramakumar
Pepine, Carl J.
Raizada, Mohan K.
Yang, Tao
Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes
title Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes
title_full Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes
title_fullStr Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes
title_full_unstemmed Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes
title_short Host‐Microbiota Communication in Spontaneously Hypertensive Rats Generates Unique IgA‐Coated Gut Microbes
title_sort host‐microbiota communication in spontaneously hypertensive rats generates unique iga‐coated gut microbes
topic Brief Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10111478/
https://www.ncbi.nlm.nih.gov/pubmed/36752270
http://dx.doi.org/10.1161/JAHA.122.027918
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