Hughes, Kevin R., Harnisch, Lukas C., Alcon-Giner, Cristina, Mitra, Suparna, Wright, Chris J., Ketskemety, Jennifer, van Sinderen, Douwe, Watson, Alastair J. M. ORCID: https://orcid.org/0000-0003-3326-0426 and Hall, Lindsay J. ORCID: https://orcid.org/0000-0001-8938-5709 (2017) Bifidobacterium breve reduces apoptotic epithelial cell shedding in an exopolysaccharide and MyD88-dependent manner. Inflammatory Bowel Diseases, 7 (1). ISSN 1078-0998
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Abstract
Certain members of the microbiota genus Bifidobacterium, are known to positively influence host well-being. Importantly, reduced bifidobacterial levels are associated with Inflammatory Bowel Disease (IBD) patients, who also have impaired epithelial barrier function, including elevated rates of apoptotic extrusion of small intestinal epithelial cells from villi; a process, termed ‘cell shedding’. Using a mouse model of pathological cell shedding, we show that mice receiving B. breve UCC2003 exhibit significantly reduced rates of small intestinal epithelial cell shedding. Bifidobacterial-induced protection appears to be mediated by a specific bifidobacterial surface exopolysaccharide and interactions with host MyD88 resulting in downregulation of intrinsic and extrinsic apoptotic responses to protect epithelial cells under highly apoptotic conditions. Our results reveal an important and previously undescribed role for B. breve, in positively modulating epithelial cell shedding outcomes via bacterial- and host-dependent factors, supporting the notion that manipulation of the microbiota affects intestinal disease outcomes.
Item Type: | Article |
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Uncontrolled Keywords: | bifidobacterium,epithelial cell shedding,inflammatory bowel disease,exopolysaccharide (eps) |
Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Groups > Gastroenterology and Gut Biology |
Depositing User: | Pure Connector |
Date Deposited: | 08 Dec 2016 00:07 |
Last Modified: | 22 Aug 2023 00:14 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/61650 |
DOI: | 10.1098/rsob.160155 |
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