Is there a role for gut microbiota in type 1 diabetes pathogenesis?

Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to t...

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Veröffentlicht in:Annals of medicine (Helsinki) Jg. 49; H. 1; S. 11 - 22
Hauptverfasser: Bibbò, Stefano, Dore, Maria Pina, Pes, Giovanni Mario, Delitala, Giuseppe, Delitala, Alessandro P.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: England Taylor & Francis 02.01.2017
Schlagworte:
Animals
autoimmunity
Autoimmunity - physiology
Diabetes Mellitus, Type 1 - immunology
Diabetes Mellitus, Type 1 - microbiology
Diabetes Mellitus, Type 1 - physiopathology
Diet - adverse effects
Dysbiosis
Dysbiosis - immunology
Gastrointestinal Microbiome - immunology
gut permeability
Humans
Insulin-Secreting Cells - immunology
Insulin-Secreting Cells - pathology
Intestines - immunology
Intestines - microbiology
Microbiota
Models, Animal
Permeability
prevention
probiotic
Probiotics - therapeutic use
therapy
type 1 diabetes mellitus
type 1 diabetes mellitus
probiotic
autoimmunity
gut permeability
therapy
Dysbiosis
prevention
ISSN:0785-3890, 1365-2060, 1365-2060
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Zusammenfassung:Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to the risk of developing the disorder. In the last years, gut microbiota has been proposed as a main factor in T1D pathogenesis. Several alterations of gut microbiota composition were described both in animal model and in humans. The decrease of Firmicutes/Bacteroides ratio was the most frequent pattern described, in particular, in human studies. Furthermore, Bacteroides, Clostridium cluster XIVa, Lactobacillus, Bifidobacterium, and Prevotella relative abundances were different in healthy and affected subjects. Dysbiosis would seem to increase intestinal permeability and thus promote the development of a pro-inflammatory niche that stimulates β-cell autoimmunity in predisposed subjects. Preliminary studies on animal models were realized to investigate the role of gut microbiota modulation as therapy or prevention approach in predisposed animals: promising and stimulating results have been reported. Key message Dietary antigens and microbiota-derived products might act as triggers of T1D by causing a pro-inflammatory and metabolic dysfunctional environment.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:0785-3890
1365-2060
1365-2060
DOI:10.1080/07853890.2016.1222449