Duodenal Mucosa of Patients With Type 1 Diabetes Shows Distinctive Inflammatory Profile and Microbiota

Pellegrini, Silvia; Sordi, Valeria; Bolla, Andrea Mario; Saita, Diego; Ferrarese, Roberto; Canducci, Filippo; Clementi, Massimo; Invernizzi, Francesca; Mariani, Alberto; Bonfanti, Riccardo; Barera, Graziano; Testoni, Pier Alberto; Doglioni, Claudio; Bosi, Emanuele; Piemonti, Lorenzo

doi:10.1210/jc.2016-3222

Cited by 117 publications

(103 citation statements)

References 37 publications

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“…As the microbiome is highly influential in the development and activity of the immune system within the gut, researchers have sought to determine the role of intestinal immune function in the development of T1D. In humans with T1D, duodenal samples had increased expression of pro-inflammatory cytokines, increased leukocytic infiltration, as well as alterations in microbial populations within the microbiome (increase in Firmicutes), which all contributed to a pro-inflammatory environment as compared to healthy controls [201]. …”

Section: Barrier Pathophysiology In Diseasementioning

confidence: 99%

Epithelial Barrier Function in Gut-Bone Signaling

Rios‐Arce

Collins

Schepper

et al. 2017

Advances in Experimental Medicine and Biology

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The intestinal epithelial barrier plays an essential role in maintaining host homeostasis. The barrier regulates nutrient absorption as well as prevents the invasion of pathogenic bacteria in the host. It is composed of epithelial cells, tight junctions, and a mucus layer. Several factors, such as cytokines, diet, and diseases can affect this barrier. These factors have been shown to increase intestinal permeability, inflammation, and translocation of pathogenic bacteria. In addition, dysregulation of the epithelial barrier can result in inflammatory diseases such as inflammatory bowel disease. Our lab and others have also shown that barrier disruption can have systemic effects including bone loss. In this chapter, we will discuss the current literature to understand the link between intestinal barrier and bone. We will discuss how inflammation, aging, dysbiosis and metabolic diseases can affect intestinal barrier-bone link. In addition, we will highlight the current suggested mechanism between intestinal barrier and bone.

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Section: Barrier Pathophysiology In Diseasementioning

confidence: 99%

Epithelial Barrier Function in Gut-Bone Signaling

Rios‐Arce

Collins

Schepper

et al. 2017

Advances in Experimental Medicine and Biology

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“…The COX2 and NOS3 gene polymorphisms alter COX2 and NOS3 gene expression, as well as cyclooxygenase and nitric oxide synthesis. Cyclooxygenase and nitric oxide are important mediators of the inflammatory response in diabetes . Low grade inflammation has been shown to play a significant role in the pathogenesis of GDM …”

Section: Discussionmentioning

confidence: 99%

COX2 and NOS3 gene polymorphisms in women with gestational diabetes

Tarnowski

Tkacz

Dziedziejko

et al. 2017

The Journal of Gene Medicine

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“…During the 1970s and 1980s, Staphylococcus aureus was unusual in the infantile intestinal microflora in Sweden; in sharp contrast, this bacteria today occurs in high numbers in the intestinal flora of 70% of Swedish children during their first year of life . Similarly, a recent study of duodenal biopsies from people with longstanding T1D showed an increased ratio of Firmicutes/Bacteroidetes, mainly because of an increase in bacilli ( Streptococcus ) . The authors concluded that a specific microbial composition of the duodenal mucosa could be a pathogenic feature of T1D .…”

Section: Why Are Other Mammals Not Affected By the Characteristic T1dmentioning

confidence: 97%

Aetiology of type 1 diabetes: Physiological growth in children affects disease progression

Skog

Korsgren

2017

Diabetes Obesity Metabolism

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The prevailing view is that type 1 diabetes (T1D) develops as a consequence of a severe decline in β-cell mass resulting from T-cell-mediated autoimmunity; however, progression from islet autoantibody seroconversion to overt diabetes and finally to total loss of C-peptide production occurs in most affected individuals only slowly over many years or even decades. This slow disease progression should be viewed in relation to the total β-cell mass of only 0.2 to 1.5 g in adults without diabetes. Focal lesions of acute pancreatitis with accumulation of leukocytes, often located around the ducts, are frequently observed in people with recent-onset T1D, and most patients display extensive periductal fibrosis, the end stage of inflammation. An injurious inflammatory adverse event, occurring within the periductal area, may have negative implications for islet neogenesis, dependent on stem cells residing within or adjacent to the ductal epithelium. This could in part prevent the 30-fold increase in β-cell mass that would normally occur during the first 20 years of life. This increase occurs in order to maintain glucose metabolism during the physiological increases in insulin production that are required to balance the 20-fold increase in body weight during childhood and increased insulin resistance during puberty. Failure to expand β-cell mass during childhood would lead to clinically overt T1D and could help to explain the apparently more aggressive form of T1D occurring in growing children when compared with that observed in affected adults.

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Duodenal Mucosa of Patients With Type 1 Diabetes Shows Distinctive Inflammatory Profile and Microbiota

Cited by 117 publications

References 37 publications

Epithelial Barrier Function in Gut-Bone Signaling

Epithelial Barrier Function in Gut-Bone Signaling

COX2 and NOS3 gene polymorphisms in women with gestational diabetes

Aetiology of type 1 diabetes: Physiological growth in children affects disease progression

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