Perivascular B cells link intestinal angiogenesis to immunity and to the gut-brain axis during neuroinflammation.

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Version: Final published version
License: CC BY 4.0
Serval ID
serval:BIB_4306784A3122
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Perivascular B cells link intestinal angiogenesis to immunity and to the gut-brain axis during neuroinflammation.
Journal
Journal of autoimmunity
Author(s)
Peter B., Rebeaud J., Vigne S., Bressoud V., Phillips N., Ruiz F., Petrova T.V., Bernier-Latmani J., Pot C.
ISSN
1095-9157 (Electronic)
ISSN-L
0896-8411
Publication state
Published
Issued date
09/2024
Peer-reviewed
Oui
Volume
148
Pages
103292
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
Disruption of gut barrier function and intestinal immune cell homeostasis are increasingly considered critical players in pathogenesis of extra-intestinal inflammatory diseases, including multiple sclerosis (MS) and its prototypical animal model, the experimental autoimmune encephalomyelitis (EAE). Breakdown of epithelial barriers increases intestinal permeability and systemic dissemination of microbiota-derived molecules. However, whether the gut-vascular barrier (GVB) is altered during EAE has not been reported. Here, we demonstrate that endothelial cell proliferation and vessel permeability increase before EAE clinical onset, leading to vascular remodeling and expansion of intestinal villi capillary bed during disease symptomatic phase in an antigen-independent manner. Concomitant to onset of angiogenesis observed prior to neurological symptoms, we identify an increase of intestinal perivascular immune cells characterized by the surface marker lymphatic vessel endothelial hyaluronic acid receptor 1 (LYVE-1). LYVE-1 <sup>+</sup> is expressed more frequently on B cells that show high levels of CD73 and have proangiogenic properties. B cell depletion was sufficient to mitigate enteric blood endothelial cell proliferation following immunization for EAE. In conclusion, we propose that altered intestinal vasculature driven by a specialized LYVE-1 <sup>+</sup> B cell subset promotes angiogenesis and that loss of GVB function is implicated in EAE development and autoimmunity.
Keywords
Animals, Mice, Encephalomyelitis, Autoimmune, Experimental/immunology, Encephalomyelitis, Autoimmune, Experimental/pathology, Encephalomyelitis, Autoimmune, Experimental/metabolism, B-Lymphocytes/immunology, B-Lymphocytes/metabolism, Brain-Gut Axis/immunology, Neovascularization, Pathologic/immunology, Endothelial Cells/immunology, Endothelial Cells/metabolism, Neuroinflammatory Diseases/immunology, Neuroinflammatory Diseases/etiology, Neuroinflammatory Diseases/pathology, Neuroinflammatory Diseases/metabolism, Disease Models, Animal, Intestinal Mucosa/immunology, Intestinal Mucosa/pathology, Intestinal Mucosa/metabolism, Intestines/immunology, Intestines/blood supply, Intestines/pathology, Mice, Inbred C57BL, Cell Proliferation, Female, Multiple Sclerosis/immunology, Multiple Sclerosis/pathology, Multiple Sclerosis/metabolism, Angiogenesis, B cell, Experimental autoimmune encephalomyelitis, Gut-brain axis, Gut–vascular barrier, Neuroinflammation
Pubmed
Web of science
Open Access
Yes
Create date
05/08/2024 17:07
Last modification date
24/09/2024 7:22
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