scholarly journals Oral Probiotic VSL#3 Prevents Autoimmune Diabetes by Modulating Microbiota and Promoting Indoleamine 2,3-Dioxygenase-Enriched Tolerogenic Intestinal Environment

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Jayashree Dolpady ◽  
Chiara Sorini ◽  
Caterina Di Pietro ◽  
Ilaria Cosorich ◽  
Roberto Ferrarese ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Inflammation ◽  
Autoimmune Diabetes ◽  
Oral Treatment ◽  
Nod Mice ◽  
Dietary Factors ◽  
Immune Homeostasis ◽  
Indoleamine 2,3 Dioxygenase ◽  
New Therapeutic Approaches ◽  
Gut Immunity

The gut microbiota modulates the autoimmune pathogenesis of type 1 diabetes (T1D) via mechanisms that remain largely unknown. The inflammasome components are innate immune sensors that are highly influenced by the gut environment and play pivotal roles in maintaining intestinal immune homeostasis. In this study we show that modifications of the gut microbiota induced by oral treatment with Lactobacillaceae-enriched probiotic VSL#3, alone or in combination with retinoic acid (RA), protect NOD mice from T1D by affecting inflammasome at the intestinal level. In particular, we show that VSL#3 treatment inhibits IL-1βexpression while enhancing release of protolerogenic components of the inflammasome, such as indoleamine 2,3-dioxygenase (IDO) and IL-33. Those modifications of the intestinal microenvironment in VSL#3-treated NOD mice modulate gut immunity by promoting differentiation of tolerogenic CD103+DCs and reducing differentiation/expansion of Th1 and Th17 cells in the intestinal mucosa and at the sites of autoimmunity, that is, within the pancreatic lymph nodes (PLN) of VSL#3-treated NOD mice. Our data provide a link between dietary factors, microbiota composition, intestinal inflammation, and immune homeostasis in autoimmune diabetes and could pave the way for new therapeutic approaches aimed at changing the intestinal microenvironment with probiotics to counterregulate autoimmunity and prevent T1D.

scholarly journals Postnatal Hematopoiesis and Gut Microbiota in NOD Mice Deviate from C57BL/6 Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Dina Silke Malling Damlund ◽  
Stine Broeng Metzdorff ◽  
Jane Preuss Hasselby ◽  
Maria Wiese ◽  
Mia Lundsager ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Adaptive Immunity ◽  
Early Life ◽  
Autoimmune Diabetes ◽  
Nod Mice ◽  
Mouse Strains ◽  
Newborn Mice ◽  
Nonobese Diabetic ◽  
Splenic Cell ◽  
Cell Profile

Neonatal studies in different mouse strains reveal that early life colonization affects the development of adaptive immunity in mice. The nonobese diabetic (NOD) mouse spontaneously develops autoimmune diabetes, but neonatal studies of NOD mice are lacking. We hypothesized that NOD mice deviate from another much used mouse strain, C57BL/6, with respect to postnatal microbiota and/or hematopoiesis and compared this in newborn mice of dams housed under the same conditions. A distinct bacteria profile rich instaphylococciwas found at postnatal days (PND) 1–4 in NOD mice. Furthermore, a distinct splenic cell profile high in a granulocytic phenotype was evident in the neonatal NOD mice whereas neonatal C57BL/6 mice showed a profile rich in monocytes. Neonatal expression ofReg3gandMuc2in the gut was deviating in NOD mice and coincided with fewer bacteria attaching to the Mucosal surface in NOD compared to C57BL/6 mice.

Killer Treg restore immune homeostasis and suppress autoimmune diabetes in prediabetic NOD mice

2011 ◽  
Vol 37 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Ayelet Kaminitz ◽  
Esma S. Yolcu ◽  
Jerry Stein ◽  
Isaac Yaniv ◽  
Haval Shirwan ◽  
...  
Keyword(s):  
Autoimmune Diabetes ◽  
Nod Mice ◽  
Immune Homeostasis

scholarly journals Dietary Composition and Effects in Inflammatory Bowel Disease

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1398 ◽  
Author(s):  
Fernando Castro ◽  
Heitor S. P. de Souza
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Dietary Habits ◽  
Intestinal Inflammation ◽  
Dietary Factors ◽  
Food Components ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

Dramatic changes in the environment and human lifestyle have been associated with the rise of various chronic complex diseases, such as inflammatory bowel disease (IBD). A dysbiotic gut microbiota has been proposed as a crucial pathogenic element, contributing to immune imbalances and fostering a proinflammatory milieu, which may be associated with disease relapses or even the initiation of IBD. In addition to representing important regulators of the mucosal immunity and the composition of the gut microbiota, food components have been shown to be potential environmental triggers of epigenetic modifications. In the context of chronic intestinal inflammation, dietary habits and specific food components have been implicated as important modulators of epigenetic mechanisms, including DNA methylation, which may predispose a person to the increased risk of the initiation and evolution of IBD. This review provides novel insights about how dietary factors may interact with the intestinal mucosa and modulate immune homeostasis by shaping the intestinal ecosystem, as well as the potential influence of diet in the etiopathogenesis and management of IBD.

scholarly journals Diet–Microbiota Interactions in Inflammatory Bowel Disease

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1533
Author(s):  
Kohei Sugihara ◽  
Nobuhiko Kamada
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Current Knowledge ◽  
Chronic Inflammatory Disease ◽  
Host Cells ◽  
Intestinal Homeostasis ◽  
New Therapeutic Approaches ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD is largely unknown, it is widely thought that diet contributes to the development of IBD. Diet shapes the composition of the gut microbiota, which plays critical roles in intestinal homeostasis. In contrast, intestinal inflammation induces gut dysbiosis and may affect the use of dietary nutrients by host cells and the gut microbiota. The interaction of diet and the gut microbiota is perturbed in patients with IBD. Herein, we review the current knowledge of diet and gut microbiota interaction in intestinal homeostasis. We also discuss alterations of diet and gut microbiota interaction that influence the outcome and the nutritional treatment of IBD. Understanding the complex relationships between diet and the gut microbiota provides crucial insight into the pathogenesis of IBD and advances the development of new therapeutic approaches.

Indoleamine 2,3 dioxygenase downregulates intestinal inflammation

2001 ◽  
Vol 120 (5) ◽  
pp. A182-A182
Author(s):  
G GREGORY ◽  
W STENSON ◽  
R NEWBERRY
Keyword(s):  
Intestinal Inflammation ◽  
Indoleamine 2,3 Dioxygenase

Prevention of autoimmune diabetes with lymphotoxin in NOD mice

Diabetes ◽  
1993 ◽  
Vol 42 (3) ◽  
pp. 398-404 ◽  
Author(s):  
H. Seino ◽  
K. Takahashi ◽  
J. Satoh ◽  
X. P. Zhu ◽  
M. Sagara ◽  
...  
Keyword(s):  
Autoimmune Diabetes ◽  
Nod Mice

InsB9-23 Gene Transfer To Hepatocytes-Based Combined Therapy Abrogates Recurrence of Type-1 Diabetes After Islet Transplantation

2020 ◽  
Author(s):  
Ada Admin ◽  
Fabio Russo ◽  
Antonio Citro ◽  
Giorgia Squeri ◽  
Francesca Sanvito ◽  
...  
Keyword(s):  
T Regulatory Cells ◽  
Lentiviral Vector ◽  
Autoimmune Diabetes ◽  
Therapeutic Option ◽  
Combined Therapy ◽  
Cell Mass ◽  
Nod Mice ◽  
Β Cell ◽  
Suboptimal Dose ◽  
Islets Transplantation

The induction of antigen (Ag)-specific tolerance represents a therapeutic option for autoimmune diabetes. We demonstrated that administration of lentiviral vector enabling expression of insulinB9-23 (LV.InsB) in hepatocytes, arrests β cell destruction in pre-diabetic NOD mice, by generating InsB9-23-specific FoxP3+T regulatory cells (Tregs). LV.InsB in combination with a suboptimal dose of anti-CD3 mAb (combined therapy, 1X5µg CT5) reverts diabetes and prevents recurrence of autoimmunity following islets transplantation in ~50% of NOD mice. We investigated whether CT optimization could lead to abrogation of recurrence of autoimmunity. Therefore, allo-islets were transplanted after optimized CT tolerogenic conditioning (1X25µg CT25). Diabetic NOD mice conditioned with CT25 when glycaemia was <500mg/dL, remained normoglycaemic for 100 days after allo-islets transplantation, displayed reduced insulitis, but independently from the graft. Accordingly, cured mice showed T cell unresponsiveness to InsB9-23 stimulation and increased Tregs frequency in islets infiltration and pancreatic LN. Additional studies revealed a complex mechanism of Ag-specific immune regulation driven by CT25, in which both Tregs and PDL1 co-stimulation cooperate to control diabetogenic cells, while transplanted islets play a crucial role, although transient, recruiting diabetogenic cells. Therefore, CT25 before allo-islets transplantation represents an Ag-specific immunotherapy to resolve autoimmune diabetes in the presence of residual endogenous β cell mass.

Sign in / Sign up

Export Citation Format

Share Document