Estela Rosell-Mases, Spain

University of Lleida / IRBLleida Experimental Medicine
Estela Rosell Mases received her B. S. in Biotechnology and M. S. in Biotechnology in Health Sciences from Universitat de Lleida (UdL). After that, she started her PhD thesis in Immunology in the Grup d’Immunologia i Immunopatologia (GRIIP) of UdL, under the supervision of Dr. Joan Verdaguer. Her thesis co-director is Dr. Chaysavanh Manichanh from the Metagenomics Lab of Vall d’Hebron Institut de Recerca (VHIR). Her PhD is focused on the connection between gut microbiota and type 1 diabetes (T1D) in mouse models. Being awarded a fellowship from Generalitat de Catalunya (FI-DGR), she received a second competitive grant from the Spanish Government (FPU). In recent years, and as part of the group led by Dr. Joan Verdaguer, Estela developed in vivo assays of a T1D immunotherapy for the biotechnology company Ahead Therapeutics. She is currently employed as associate professor while finishing her PhD studies.

Presenter of 1 Presentation

 Conference Calendar

116C-NOD GUT MICROBIOTA MODULATES TH RESPONSE AND AUTOIMMUNE DIABETES INCIDENCE OF NOD MICE

Session Name
PS52- TYPE 1 DIABETES MELLITUS
Session Type
PARALLEL SESSIONS
Date
31.05.2021, Monday
Session Time
13:30 - 15:30
Room
HALL F
Lecture Time
14:50 - 15:00
Presenter
Session Icon
Pre Recorded

Abstract

Background and Aims

The association between gut microbiota alterations and beta cell autoimmunity in type 1 diabetes (T1D) has been suggested by both animal model experiments and clinical studies. However, the adaptive immune system modulation exerted by the gut microbiota in the context of T1D remains poorly understood. To explore this issue, the islet beta cell-autoreactive B lymphocyte transgenic 116C-NOD mouse model, which surprisingly displays a decreased T1D incidence compared with NOD mouse, was used. Our objective was to analyze the effect of the 116C-NOD gut microbiota natural transfer on the immune phenotype, the intestinal microbial composition, and the progress of T1D in recipient NOD mice.

Methods

To achieve this goal, NOD mice were kept in isolation (isoNOD) or cohousing (coNOD) conditions regarding their transgenic 116C-NOD siblings. Fecal microbiome composition was analyzed using 16S rRNA gene sequencing. Immunological studies included B and T cell cytokine secretion profiling and population characterization after culture. T1D development was monitored by measuring glycosuria and glycaemia.

Results

Microbiome analysis revealed that coNOD harboured a different microbial profile compared with isoNOD mice. As for their immune phenotype, lymphocytes from coNOD mice developed a Th1/Th17 response, intermediate between the predominant Th1 pattern of isoNOD and the prevalent Th17 profile of 116C-NOD model. Furthermore, coNOD mice showed a significantly lower disease incidence than their isoNOD counterparts.

Conclusions

Taken together, these results suggest that 116C-NOD gut microbiota, previously tuned by the own 116C-NOD lymphocyte repertoire, may modify T1D development of recipient NOD mice through a Th status shift.

Hide