Gliadin Nanoparticles Induce Immune Tolerance to Gliadin in Mouse Models of Celiac Disease.


Journal

Gastroenterology
ISSN: 1528-0012
Titre abrégé: Gastroenterology
Pays: United States
ID NLM: 0374630

Informations de publication

Date de publication:
05 2020
Historique:
received: 28 06 2019
revised: 26 01 2020
accepted: 27 01 2020
pubmed: 8 2 2020
medline: 21 10 2020
entrez: 8 2 2020
Statut: ppublish

Résumé

Celiac disease could be treated, and potentially cured, by restoring T-cell tolerance to gliadin. We investigated the safety and efficacy of negatively charged 500-nm poly(lactide-co-glycolide) nanoparticles encapsulating gliadin protein (TIMP-GLIA) in 3 mouse models of celiac disease. Uptake of these nanoparticles by antigen-presenting cells was shown to induce immune tolerance in other animal models of autoimmune disease. We performed studies with C57BL/6; RAG1 TIMP-GLIA did not increase markers of maturation on cultured human dendritic cells or induce activation of T cells from patients with active or treated celiac disease. In the delayed-type hypersensitivity (model 1), the HLA-DQ8 transgenic (model 2), and the gliadin memory T-cell enteropathy (model 3) models of celiac disease, intravenous injections of TIMP-GLIA significantly decreased gliadin-specific T-cell proliferation (in models 1 and 2), inflammatory cytokine secretion (in models 1, 2, and 3), circulating gliadin-specific IgG/IgG2c (in models 1 and 2), ear swelling (in model 1), gluten-dependent enteropathy (in model 3), and body weight loss (in model 3). In model 1, the effects were shown to be dose dependent. Splenocytes from HLA-DQ8 transgenic mice given TIMP-GLIA nanoparticles, but not control nanoparticles, had increased levels of FOXP3 and gene expression signatures associated with tolerance induction. In mice with gliadin sensitivity, injection of TIMP-GLIA nanoparticles induced unresponsiveness to gliadin and reduced markers of inflammation and enteropathy. This strategy might be developed for the treatment of celiac disease.

Sections du résumé

BACKGROUND & AIMS
Celiac disease could be treated, and potentially cured, by restoring T-cell tolerance to gliadin. We investigated the safety and efficacy of negatively charged 500-nm poly(lactide-co-glycolide) nanoparticles encapsulating gliadin protein (TIMP-GLIA) in 3 mouse models of celiac disease. Uptake of these nanoparticles by antigen-presenting cells was shown to induce immune tolerance in other animal models of autoimmune disease.
METHODS
We performed studies with C57BL/6; RAG1
RESULTS
TIMP-GLIA did not increase markers of maturation on cultured human dendritic cells or induce activation of T cells from patients with active or treated celiac disease. In the delayed-type hypersensitivity (model 1), the HLA-DQ8 transgenic (model 2), and the gliadin memory T-cell enteropathy (model 3) models of celiac disease, intravenous injections of TIMP-GLIA significantly decreased gliadin-specific T-cell proliferation (in models 1 and 2), inflammatory cytokine secretion (in models 1, 2, and 3), circulating gliadin-specific IgG/IgG2c (in models 1 and 2), ear swelling (in model 1), gluten-dependent enteropathy (in model 3), and body weight loss (in model 3). In model 1, the effects were shown to be dose dependent. Splenocytes from HLA-DQ8 transgenic mice given TIMP-GLIA nanoparticles, but not control nanoparticles, had increased levels of FOXP3 and gene expression signatures associated with tolerance induction.
CONCLUSIONS
In mice with gliadin sensitivity, injection of TIMP-GLIA nanoparticles induced unresponsiveness to gliadin and reduced markers of inflammation and enteropathy. This strategy might be developed for the treatment of celiac disease.

Identifiants

pubmed: 32032584
pii: S0016-5085(20)30157-8
doi: 10.1053/j.gastro.2020.01.045
pmc: PMC7198359
mid: NIHMS1568962
pii:
doi:

Substances chimiques

HLA-DQ Antigens 0
HLA-DQ8 antigen 0
Polyglactin 910 34346-01-5
Glutens 8002-80-0
Gliadin 9007-90-3

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1667-1681.e12

Subventions

Organisme : NIBIB NIH HHS
ID : R01 EB013198
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS099334
Pays : United States

Informations de copyright

Copyright © 2020 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Auteurs

Tobias L Freitag (TL)

Department of Bacteriology and Immunology, University of Helsinki, Finland; Translational Immunology Research Program, University of Helsinki, Finland. Electronic address: tobias.Freitag@helsinki.fi.

Joseph R Podojil (JR)

Department of Microbiology and Immunology, Northwestern University, Chicago, Illinois; Cour Pharmaceutical Development Company, Northbrook, Illinois.

Ryan M Pearson (RM)

Cour Pharmaceutical Development Company, Northbrook, Illinois; Department of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan.

Frank J Fokta (FJ)

Cour Pharmaceutical Development Company, Northbrook, Illinois.

Cecilia Sahl (C)

Department of Bacteriology and Immunology, University of Helsinki, Finland.

Marcel Messing (M)

Department of Bacteriology and Immunology, University of Helsinki, Finland; Translational Immunology Research Program, University of Helsinki, Finland.

Leif C Andersson (LC)

Department of Pathology, University of Helsinki, Finland.

Katarzyna Leskinen (K)

Translational Immunology Research Program, University of Helsinki, Finland.

Päivi Saavalainen (P)

Translational Immunology Research Program, University of Helsinki, Finland.

Lisa I Hoover (LI)

Precision for Medicine, Frederick, Maryland.

Kelly Huang (K)

Precision for Medicine, Frederick, Maryland.

Deborah Phippard (D)

Precision for Medicine, Frederick, Maryland.

Sanaz Maleki (S)

Discipline of Pathology, School of Medical Sciences, Bosch Institute, Sydney Medical School, University of Sydney, Sydney, Australia.

Nicholas J C King (NJC)

Discipline of Pathology, School of Medical Sciences, Bosch Institute, Sydney Medical School, University of Sydney, Sydney, Australia.

Lonnie D Shea (LD)

Department of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan.

Stephen D Miller (SD)

Department of Microbiology and Immunology, Northwestern University, Chicago, Illinois; Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Seppo K Meri (SK)

Department of Bacteriology and Immunology, University of Helsinki, Finland; Translational Immunology Research Program, University of Helsinki, Finland.

Daniel R Getts (DR)

Department of Microbiology and Immunology, Northwestern University, Chicago, Illinois; Cour Pharmaceutical Development Company, Northbrook, Illinois; Discipline of Pathology, School of Medical Sciences, Bosch Institute, Sydney Medical School, University of Sydney, Sydney, Australia; Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

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Classifications MeSH