Mutual modulation of gut microbiota and the immune system in type 1 diabetes models

Estela Rosell-Mases, Alba Santiago, Marta Corral-Pujol, Francisca Yáñez, Encarna Varela, Leire Egia-Mendikute, Berta Arpa, Catalina Cosovanu, Anaïs Panosa, Gerard Serrano-Gómez, Conchi Mora, Joan Verdaguer () and Chaysavanh Manichanh ()
Additional contact information
Estela Rosell-Mases: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Alba Santiago: Vall d’Hebron Barcelona Hospital Campus
Marta Corral-Pujol: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Francisca Yáñez: Vall d’Hebron Barcelona Hospital Campus
Encarna Varela: Vall d’Hebron Barcelona Hospital Campus
Leire Egia-Mendikute: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Berta Arpa: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Catalina Cosovanu: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Anaïs Panosa: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Gerard Serrano-Gómez: Vall d’Hebron Barcelona Hospital Campus
Conchi Mora: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Joan Verdaguer: Universitat de Lleida (UdL) and Institut de Recerca Biomèdica de Lleida (IRBLleida)
Chaysavanh Manichanh: Vall d’Hebron Barcelona Hospital Campus

Nature Communications, 2023, vol. 14, issue 1, 1-18

Abstract: Abstract The transgenic 116C-NOD mouse strain exhibits a prevalent Th17 phenotype, and reduced type 1 diabetes (T1D) compared to non-obese diabetic (NOD) mice. A cohousing experiment between both models revealed lower T1D incidence in NOD mice cohoused with 116C-NOD, associated with gut microbiota changes, reduced intestinal permeability, shifts in T and B cell subsets, and a transition from Th1 to Th17 responses. Distinct gut bacterial signatures were linked to T1D in each group. Using a RAG-2−/− genetic background, we found that T cell alterations promoted segmented filamentous bacteria proliferation in young NOD and 116C-NOD, as well as in immunodeficient NOD.RAG-2−/− and 116C-NOD.RAG-2−/− mice across all ages. Bifidobacterium colonization depended on lymphocytes and thrived in a non-diabetogenic environment. Additionally, 116C-NOD B cells in 116C-NOD.RAG-2−/− mice enriched the gut microbiota in Adlercreutzia and reduced intestinal permeability. Collectively, these results indicate reciprocal modulation between gut microbiota and the immune system in rodent T1D models.

Date: 2023
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-023-43652-x Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-43652-x

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-023-43652-x

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().