Type 1 Diabetes and Associated Immune-Mediated Diseases: Focus on Environmental Factors

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 2972

Special Issue Editors


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Guest Editor
Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague and Novy Hradek, Prague, Czech Republic
Interests: immunology; diabetes; microbiota; metabolites; associated immune-mediated diseases

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Guest Editor
Haupt-Jørgensen Group, Bartholin Institute, Department of Pathology, Rigshospitaet, Ole Maaløes Vej 5, Building 2, 3 floor, 2200 Copenhagen N, Denmark
Interests: Type 1 diabetes; celiac disease; intestinal permeability; Enterovirus; Gluten-Free Diet; Innate immune system; Beta cell; beta-cell stress; islet of Langerhans; NOD mouse

Special Issue Information

Dear Colleagues,

Type 1 diabetes (T1D) is an autoimmune disease in which environmental factors play an important role, as documented by the remarkably growing T1D incidence in developed countries and decreasing age of disease onset in recent decades. Pathogenic, effector, and regulatory immune responses may all be influenced by the environment, but due to their complexities and variability, these interactions are difficult to dissect and to define, yet they represent a promising and relatively safe approach in disease prevention or arrest. Infections, dietary factor, intestinal microbiota, metabolism and metabolites, and their interplays are capable of shaping preferentially mucosal, adaptive and innate immune responses. 

The aim of this Special Issue is thus to focus attention on the immune mechanisms as well as interplays with environmental factors in T1D. This is, however, also relevant in many other immune-mediated diseases with different genetic predispositions and initial etiopathogenic hits. Therefore,  the focus of this Special  Issue is on the role of immunity, diets, microbiota, and/or metabolites  not confined only to T1D, but also including T1D-associated autoimmune diseases such as celiac disease, autoimmune thyroid disease, autoimmune gastritis, pernicious anemia, Sjogren's syndrome, as well as other immune-mediated diseases (e.g., psoriasis or Parkinson's disease) in which parallels in terms of the role of immunity and the environment may be found.  

In this Special Issue, we invite scientists to contribute all article types published in Cells and within the framework of the above-described aims.

Dr. David Funda
Dr. Martin Haupt-Jorgensen
Guest Editors

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Keywords

  • type 1 diabetes
  • immune mechanisms
  • environmental factors
  • infection
  • diets
  • microbiota
  • metabolites
  • associated immune-mediated diseases

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Published Papers (1 paper)

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Research

15 pages, 2273 KiB  
Article
A Gluten-Free Diet during Pregnancy and Early Life Increases Short Chain Fatty Acid-Producing Bacteria and Regulatory T Cells in Prediabetic NOD Mice
by Valdemar Brimnes Ingemann Johansen, Daisy Færø, Karsten Buschard, Karsten Kristiansen, Flemming Pociot, Pia Kiilerich, Knud Josefsen, Martin Haupt-Jorgensen and Julie Christine Antvorskov
Cells 2023, 12(12), 1567; https://doi.org/10.3390/cells12121567 - 6 Jun 2023
Cited by 1 | Viewed by 2440
Abstract
The incidence of the autoimmune disease type 1 diabetes is increasing, likely caused by environmental factors. A gluten-free diet has previously been shown to ameliorate autoimmune diabetes in non-obese diabetic (NOD) mice and humans. Although the exact mechanisms are not understood, interventions influencing [...] Read more.
The incidence of the autoimmune disease type 1 diabetes is increasing, likely caused by environmental factors. A gluten-free diet has previously been shown to ameliorate autoimmune diabetes in non-obese diabetic (NOD) mice and humans. Although the exact mechanisms are not understood, interventions influencing the intestinal microbiota early in life affect the risk of type 1 diabetes. Here, we characterize how NOD mice that are fed a gluten-free (GF) diet differ from NOD mice that are fed a gluten-containing standard (STD) diet in terms of their microbiota composition by 16S rRNA gene amplicon sequencing and pancreatic immune environment by real-time quantitative PCR at the prediabetic stage at 6 and 13 weeks of age. Gut microbiota analysis revealed highly distinct microbiota compositions in both the cecum and the colon of GF-fed mice compared with STD-fed mice. The microbiotas of the GF-fed mice were characterized by an increased Firmicutes/Bacteroidetes ratio, an increased abundance of short chain fatty acid (particularly butyrate)-producing bacteria, and a reduced abundance of Lactobacilli compared with STD mice. We found that the insulitis score in the GF mice was significantly reduced compared with the STD mice and that the markers for regulatory T cells and T helper 2 cells were upregulated in the pancreas of the GF mice. In conclusion, a GF diet during pre- and early post-natal life induces shifts in the cecal and colonic microbiota compatible with a less inflammatory environment, providing a likely mechanism for the protective effect of a GF diet in humans. Full article
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