Genome analysis of Bifidobacterium adolescentis and investigation of its effects on inflammation and intestinal barrier function
Numerous studies have confirmed that gut microbiota is a key driver in the occurrence and progression of inflammatory bowel disease (IBD). Based on the bacterial collection constructed in our previous studies, we founded that Bifidobacterium adolescentis AF91-08b2A has the potential beneficial funct...
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Published in | Frontiers in microbiology Vol. 15; p. 1496280 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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22.01.2025
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Abstract | Numerous studies have confirmed that gut microbiota is a key driver in the occurrence and progression of inflammatory bowel disease (IBD). Based on the bacterial collection constructed in our previous studies, we founded that
Bifidobacterium adolescentis
AF91-08b2A has the potential beneficial function. We designed cohort studies, genomic studies and animal experiments to further explore the probiotic function of
Bifidobacterium adolescentis
AF91-08b2A and its therapeutic effect on IBD. The depletion of
B. adolescentis
in individuals with IBD suggested its significance for intestinal health. Genomic analysis highlighted the probiotic attributes of
B. adolescentis
AF91-08b2A, including resistance to antibiotics and stress, and metabolic pathways related to energy and carbohydrate metabolism, which are likely to enhance its therapeutic efficacy. In DSS-induced mice colitis model, the strain significantly enhanced the disease activity index (DAI), curbed weight loss, and attenuated colonic damage. It effectively modulated the immune response by reducing the levels of pro-inflammatory cytokines such as IL-6, IL-1β, IL-17A, IFN-γ, and TNF-α, while promoting the secretion of anti-inflammatory cytokines like IL-4, IL-10, and TGF-β1. The restoration of tight junction proteins ZO-1, occludin, and claudin-2 by
B. adolescentis
AF91-08b2A demonstrated its capacity to safeguard the intestinal epithelial barrier. Collectively, our findings indicate
B. adolescentis
AF91-08b2A as a valuable therapeutic option for UC, with its multifaceted approach to reducing inflammation and fortifying the intestinal barrier. |
---|---|
AbstractList | Numerous studies have confirmed that gut microbiota is a key driver in the occurrence and progression of inflammatory bowel disease (IBD). Based on the bacterial collection constructed in our previous studies, we founded that
Bifidobacterium adolescentis
AF91-08b2A has the potential beneficial function. We designed cohort studies, genomic studies and animal experiments to further explore the probiotic function of
Bifidobacterium adolescentis
AF91-08b2A and its therapeutic effect on IBD. The depletion of
B. adolescentis
in individuals with IBD suggested its significance for intestinal health. Genomic analysis highlighted the probiotic attributes of
B. adolescentis
AF91-08b2A, including resistance to antibiotics and stress, and metabolic pathways related to energy and carbohydrate metabolism, which are likely to enhance its therapeutic efficacy. In DSS-induced mice colitis model, the strain significantly enhanced the disease activity index (DAI), curbed weight loss, and attenuated colonic damage. It effectively modulated the immune response by reducing the levels of pro-inflammatory cytokines such as IL-6, IL-1β, IL-17A, IFN-γ, and TNF-α, while promoting the secretion of anti-inflammatory cytokines like IL-4, IL-10, and TGF-β1. The restoration of tight junction proteins ZO-1, occludin, and claudin-2 by
B. adolescentis
AF91-08b2A demonstrated its capacity to safeguard the intestinal epithelial barrier. Collectively, our findings indicate
B. adolescentis
AF91-08b2A as a valuable therapeutic option for UC, with its multifaceted approach to reducing inflammation and fortifying the intestinal barrier. Numerous studies have confirmed that gut microbiota is a key driver in the occurrence and progression of inflammatory bowel disease (IBD). Based on the bacterial collection constructed in our previous studies, we founded that Bifidobacterium adolescentis AF91-08b2A has the potential beneficial function. We designed cohort studies, genomic studies and animal experiments to further explore the probiotic function of Bifidobacterium adolescentis AF91-08b2A and its therapeutic effect on IBD. The depletion of B. adolescentis in individuals with IBD suggested its significance for intestinal health. Genomic analysis highlighted the probiotic attributes of B. adolescentis AF91-08b2A, including resistance to antibiotics and stress, and metabolic pathways related to energy and carbohydrate metabolism, which are likely to enhance its therapeutic efficacy. In DSS-induced mice colitis model, the strain significantly enhanced the disease activity index (DAI), curbed weight loss, and attenuated colonic damage. It effectively modulated the immune response by reducing the levels of pro-inflammatory cytokines such as IL-6, IL-1β, IL-17A, IFN-γ, and TNF-α, while promoting the secretion of anti-inflammatory cytokines like IL-4, IL-10, and TGF-β1. The restoration of tight junction proteins ZO-1, occludin, and claudin-2 by B. adolescentis AF91-08b2A demonstrated its capacity to safeguard the intestinal epithelial barrier. Collectively, our findings indicate B. adolescentis AF91-08b2A as a valuable therapeutic option for UC, with its multifaceted approach to reducing inflammation and fortifying the intestinal barrier. Numerous studies have confirmed that gut microbiota is a key driver in the occurrence and progression of inflammatory bowel disease (IBD). Based on the bacterial collection constructed in our previous studies, we founded that Bifidobacterium adolescentis AF91-08b2A has the potential beneficial function. We designed cohort studies, genomic studies and animal experiments to further explore the probiotic function of Bifidobacterium adolescentis AF91-08b2A and its therapeutic effect on IBD. The depletion of B. adolescentis in individuals with IBD suggested its significance for intestinal health. Genomic analysis highlighted the probiotic attributes of B. adolescentis AF91-08b2A, including resistance to antibiotics and stress, and metabolic pathways related to energy and carbohydrate metabolism, which are likely to enhance its therapeutic efficacy. In DSS-induced mice colitis model, the strain significantly enhanced the disease activity index (DAI), curbed weight loss, and attenuated colonic damage. It effectively modulated the immune response by reducing the levels of pro-inflammatory cytokines such as IL-6, IL-1β, IL-17A, IFN-γ, and TNF-α, while promoting the secretion of anti-inflammatory cytokines like IL-4, IL-10, and TGF-β1. The restoration of tight junction proteins ZO-1, occludin, and claudin-2 by B. adolescentis AF91-08b2A demonstrated its capacity to safeguard the intestinal epithelial barrier. Collectively, our findings indicate B. adolescentis AF91-08b2A as a valuable therapeutic option for UC, with its multifaceted approach to reducing inflammation and fortifying the intestinal barrier.Numerous studies have confirmed that gut microbiota is a key driver in the occurrence and progression of inflammatory bowel disease (IBD). Based on the bacterial collection constructed in our previous studies, we founded that Bifidobacterium adolescentis AF91-08b2A has the potential beneficial function. We designed cohort studies, genomic studies and animal experiments to further explore the probiotic function of Bifidobacterium adolescentis AF91-08b2A and its therapeutic effect on IBD. The depletion of B. adolescentis in individuals with IBD suggested its significance for intestinal health. Genomic analysis highlighted the probiotic attributes of B. adolescentis AF91-08b2A, including resistance to antibiotics and stress, and metabolic pathways related to energy and carbohydrate metabolism, which are likely to enhance its therapeutic efficacy. In DSS-induced mice colitis model, the strain significantly enhanced the disease activity index (DAI), curbed weight loss, and attenuated colonic damage. It effectively modulated the immune response by reducing the levels of pro-inflammatory cytokines such as IL-6, IL-1β, IL-17A, IFN-γ, and TNF-α, while promoting the secretion of anti-inflammatory cytokines like IL-4, IL-10, and TGF-β1. The restoration of tight junction proteins ZO-1, occludin, and claudin-2 by B. adolescentis AF91-08b2A demonstrated its capacity to safeguard the intestinal epithelial barrier. Collectively, our findings indicate B. adolescentis AF91-08b2A as a valuable therapeutic option for UC, with its multifaceted approach to reducing inflammation and fortifying the intestinal barrier. Numerous studies have confirmed that gut microbiota is a key driver in the occurrence and progression of inflammatory bowel disease (IBD). Based on the bacterial collection constructed in our previous studies, we founded that AF91-08b2A has the potential beneficial function. We designed cohort studies, genomic studies and animal experiments to further explore the probiotic function of AF91-08b2A and its therapeutic effect on IBD. The depletion of in individuals with IBD suggested its significance for intestinal health. Genomic analysis highlighted the probiotic attributes of AF91-08b2A, including resistance to antibiotics and stress, and metabolic pathways related to energy and carbohydrate metabolism, which are likely to enhance its therapeutic efficacy. In DSS-induced mice colitis model, the strain significantly enhanced the disease activity index (DAI), curbed weight loss, and attenuated colonic damage. It effectively modulated the immune response by reducing the levels of pro-inflammatory cytokines such as IL-6, IL-1β, IL-17A, IFN-γ, and TNF-α, while promoting the secretion of anti-inflammatory cytokines like IL-4, IL-10, and TGF-β1. The restoration of tight junction proteins ZO-1, occludin, and claudin-2 by AF91-08b2A demonstrated its capacity to safeguard the intestinal epithelial barrier. Collectively, our findings indicate AF91-08b2A as a valuable therapeutic option for UC, with its multifaceted approach to reducing inflammation and fortifying the intestinal barrier. |
Author | Zou, Yuanqiang Wang, Haoyu You, Xinbi Xia, Binbin Hu, Tongyuan Yang, Jinlong Sun, Yang Yuan, Yue Miao, Yinglei Li, Bo Wang, Mengmeng Li, Shangyong Liang, Hewei |
AuthorAffiliation | 4 College of Life Sciences, University of Chinese Academy of Sciences , Beijing , China 6 BGI Research , Wuhan , China 8 BGI Research , Kunming , China 10 Yunnan Geriatric Medical Center , Kunming , China 1 Department of Gastroenterology, The First Affiliated Hospital of Kunming Medical University , Kunming , China 3 BGI Research , Shenzhen , China 5 School of Basic Medicine, Qingdao Medical College, Qingdao University , Qingdao , China 2 Yunnan Province Clinical Research Center for Digestive Diseases , Kunming , China 7 Shenzhen Engineering Laboratory of Detection and Intervention of Human Intestinal Microbiome, BGI Research , Shenzhen , China 9 College of Forensic Science, Xi’an Jiaotong University , Xi’an , China |
AuthorAffiliation_xml | – name: 9 College of Forensic Science, Xi’an Jiaotong University , Xi’an , China – name: 3 BGI Research , Shenzhen , China – name: 1 Department of Gastroenterology, The First Affiliated Hospital of Kunming Medical University , Kunming , China – name: 10 Yunnan Geriatric Medical Center , Kunming , China – name: 6 BGI Research , Wuhan , China – name: 4 College of Life Sciences, University of Chinese Academy of Sciences , Beijing , China – name: 2 Yunnan Province Clinical Research Center for Digestive Diseases , Kunming , China – name: 8 BGI Research , Kunming , China – name: 5 School of Basic Medicine, Qingdao Medical College, Qingdao University , Qingdao , China – name: 7 Shenzhen Engineering Laboratory of Detection and Intervention of Human Intestinal Microbiome, BGI Research , Shenzhen , China |
Author_xml | – sequence: 1 givenname: Bo surname: Li fullname: Li, Bo – sequence: 2 givenname: Haoyu surname: Wang fullname: Wang, Haoyu – sequence: 3 givenname: Mengmeng surname: Wang fullname: Wang, Mengmeng – sequence: 4 givenname: Hewei surname: Liang fullname: Liang, Hewei – sequence: 5 givenname: Tongyuan surname: Hu fullname: Hu, Tongyuan – sequence: 6 givenname: Jinlong surname: Yang fullname: Yang, Jinlong – sequence: 7 givenname: Shangyong surname: Li fullname: Li, Shangyong – sequence: 8 givenname: Xinbi surname: You fullname: You, Xinbi – sequence: 9 givenname: Binbin surname: Xia fullname: Xia, Binbin – sequence: 10 givenname: Yue surname: Yuan fullname: Yuan, Yue – sequence: 11 givenname: Yuanqiang surname: Zou fullname: Zou, Yuanqiang – sequence: 12 givenname: Yinglei surname: Miao fullname: Miao, Yinglei – sequence: 13 givenname: Yang surname: Sun fullname: Sun, Yang |
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Copyright | Copyright © 2025 Li, Wang, Wang, Liang, Hu, Yang, Li, You, Xia, Yuan, Zou, Miao and Sun. Copyright © 2025 Li, Wang, Wang, Liang, Hu, Yang, Li, You, Xia, Yuan, Zou, Miao and Sun. 2025 Li, Wang, Wang, Liang, Hu, Yang, Li, You, Xia, Yuan, Zou, Miao and Sun |
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Keywords | Bifidobacterium adolescentis probiotic function intestinal barrier function inflammatory bowel disease genomic analysis |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors have contributed equally to this work Reviewed by: Zhongyue Yang, Stanford University, United States Edited by: Mitesh Patel, Parul University, India Honghua Hu, Macquarie University, Australia |
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Title | Genome analysis of Bifidobacterium adolescentis and investigation of its effects on inflammation and intestinal barrier function |
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