The Role of Gut Microbiota and Environmental Factors in Type 1 Diabetes Pathogenesis

Dedrick, Sandra; Sundaresh, Bharathi; Huang, Qian; Brady, Claudia; Yoo, Tessa; Cronin, Catherine Tracy; Rudnicki, Caitlin; Flood, Michael; Momeni, Babak; Ludvigsson, Johnny; Altındiş, Emrah

doi:10.3389/fendo.2020.00078

Cited by 108 publications

(121 citation statements)

References 272 publications

(274 reference statements)

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“…Moreover, exposure to P. (11)(12)(13)54), there is a common pattern. Specifically, the diversity of T1D patients' gut microbiome is decreased while there is an increased prevalence of Bacteriodetes taxa and an altered metabolomic profile compared to healthy controls (14). Most of these studies are observational and do not define any mechanism related to T1D onset.…”

Section: Discussionmentioning

confidence: 99%

“…Various environmental factors have been studied including diet, birth mode, infections and antibiotics; however, the roles of these factors and cause of T1D largely remain unknown (7)(8)(9). This said, recent gut microbiome studies have observed an altered microbial and metabolite composition, and increased intestinal permeability in subjects with T1D (10)(11)(12)(13)(14). In addition to gut microbes, viral infections have also been suggested to play a role in T1D, yet no studies have identified a direct causal link (15).…”

Section: Introductionmentioning

confidence: 99%

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A Gut Microbial Peptide and Molecular Mimicry in the Pathogenesis of Type 1 Diabetes

Girdhar¹,

Huang

Chow

et al. 2020

Preprint

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Type 1 Diabetes (T1D) is an autoimmune disease characterized by destruction of pancreatic β-cells. Focusing on the main insulin epitope, insulin B-chain 9-23 (insB:9-23), we explored whether a microbial insB:9-23 mimic could modulate T1D. We now demonstrate that a microbial insB:9-23 mimic of Parabacteroides distasonis, a human gut commensal, exclusively stimulates non-obese diabetic (NOD) mouse T cells specific to insB:9-23. Indeed, immunization of NOD mice with either the bacterial mimic peptide or insB:9-23 further verified the cross-reactivity in vivo. Modeling P. distasonis peptide revealed a potential pathogenic register 3 binding. P. distasonis colonization of the female NOD mice gut accelerated T1D onset. In addition, adoptive transfer of splenocytes from NOD mice colonized with P. distasonis to NOD.SCID recipients conferred the enhanced disease phenotype. Integration analysis of published infant T1D gut microbiome data revealed that P. distasonis peptide is not present in the gut microbiota in the first year of life of infants that eventually develop T1D. Furthermore, P. distasonis peptide can stimulate human T cell clones specific to insB:9-23 and T1D patients demonstrated a strong humoral immune response to P. distasonis than controls. Taken together, our studies define a potential molecular mimicry link between T1D pathogenesis and the gut microbiota.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Gut Microbial Peptide and Molecular Mimicry in the Pathogenesis of Type 1 Diabetes

Girdhar¹,

Huang

Chow

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…Accumulating evidence reported that gut microbiota were associated with multiple kinds of diseases including colon cancer [32], gestational diabetes [33], type 1 diabetes [34], cardiovascular disease [35] and so on. In addition, biological processes containing diet, weight [36], bone homeostasis [37] and postnatal development were also in uenced by gut microbiota.…”

Section: Discussionmentioning

confidence: 99%

Identification and characteristics of postnatal development-related long non-coding RNAs under microbiota dependent condition

Zheng¹,

Zhang²,

Zhang³

et al. 2020

Preprint

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BackgroundThe interplay of long-non coding RNAs (lncRNAs) and the intestinal microbiota may serve as an essential role in intestinal development and homeostasis. Microbiota could regulate a large numbers of lncRNAs expression in intestinal epithelial cells. However, the associations between lncRNAs and microbiota during early postnatal development stages are still need to understand. MethodsIn present study, the microbial effects on lncRNA of intestinal epithelial cells (IECs) during postnatal development stage were investigated. ResultsWe identified gut microbiota-specific lncRNAs in diverse postnatal development stages including week 1, week 4 and week 12/16 of mice. A large proportion of gut microbiota-specific lncRNAs only were differential expressed in a single postnatal development stage. Up- and down-regulated gut microbiota-specific lncRNAs both showed consistent expression pattern. We also constructed gut microbiota-specific lncRNAs and coding genes interacted co-expressed networks. Functional analysis indicated that gut microbiota-specific lncRNAs were associated with ABC transporters. ConclusionsIn summary, the present study characterizes the landscape of lncRNAs associated with gut microbiota in different postnatal development stages. It provide assistance for exploring the relationships among lncRNAs, gut microbiota and postnatal development stages.

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“…Infantis , which is involved in child's immunity ( 126 , 127 ). It belongs to lactic acid bacteria, Bifidobacterium and Lactobacillus , which can break down human milk oligosaccharides ( 128 ).…”

Section: Early Nutrition As Modulator Of Microbiota In Relation To T1mentioning

confidence: 99%

Early Nutrition and Risk of Type 1 Diabetes: The Role of Gut Microbiota

et al. 2020

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Type 1 diabetes (T1D) appears most frequently in childhood, with an alarming increasing incidence in the last decades. Although the genetic predisposition is a major risk factor, it cannot solely explain the complex etiology of T1D which is still not fully understood. In this paper, we reviewed the most recent findings on the role of early nutrition and the involvement of the gut microbiota in the etiopathogenesis of T1D. The main conclusions that are withdrawn from the current literature regarding alleviating the risk of developing T1D through nutrition are the encouragement of long-term breast-feeding for at least the first 6 months of life and the avoidance of early complementary foods and gluten introduction (before 4 months of age) as well as cow milk introduction before 12 months of life. These detrimental feeding habits create a gut microbiota dysbiotic state that can contribute to the onset of T1D in infancy. Finally, we discussed the possibility to introduce probiotics, prebiotics and post-biotics in the prevention of T1D.

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The Role of Gut Microbiota and Environmental Factors in Type 1 Diabetes Pathogenesis

Cited by 108 publications

References 272 publications

A Gut Microbial Peptide and Molecular Mimicry in the Pathogenesis of Type 1 Diabetes

A Gut Microbial Peptide and Molecular Mimicry in the Pathogenesis of Type 1 Diabetes

Identification and characteristics of postnatal development-related long non-coding RNAs under microbiota dependent condition

Early Nutrition and Risk of Type 1 Diabetes: The Role of Gut Microbiota

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