We assessed the effect of B. thetaiotaomicron administration on primary readouts of colitis (weight loss, histopathology, and immune parameters) in dextran sodium sulphate (DSS) and interleukin-10 knockout (IL10KO) models of IBD.
The TGF-β-induced Tregs that express IL-10 blocked colitis when transferred into the Rag/CD25<sup>-</sup> CD4<sup>+</sup> T cell transfer model of inflammatory bowel disease.
In the present study, we report a novel homozygous null mutation within interleukin-10 receptor B (IL10RB) gene in a child presenting with severe VEO-IBD.
We performed direct gene sequencing looking for 94 variations in NOD2, ATG16L1, IL23R, IL10R, IL10 and XIAP genes previously shown as correlated with IBD both in multifactorial and in Mendelian models.
cAT-MSC-secreted TSG-6 ameliorated IBD and regulated colonic expression of pro- and anti-inflammatory cytokines such as tumor necrosis factor-α, interleukin-6, and interleukin-10.
Moreover, adoptive transfer of CD69<sup>+</sup> Tregs but not CD69<sup>-</sup>Tregs or CD69<sup>+</sup> Tregs deficient in IL-10 dramatically prevented the development of inflammatory bowel disease (IBD) in mice.
<i>Bifico</i> is a probiotic mixture containing <i>Bifidobacterium</i>, <i>Lactobacillus acidophilus</i>, and <i>Enterococcus.</i> Studies support that <i>Bifico</i> has a protective effect in experimental colitis (IL-10-deficient and TNBS) models and in patients with inflammatory bowel disease (IBD).
Hematopoietic stem cell transplantation is considered the only curative therapy for very early-onset inflammatory bowel disease with specific immune defects, such as interleukin-10 receptor deficiency.
Mutations in interleukin-10 receptor (IL-10R) genes are one cause of very early-onset inflammatory bowel disease with perianal lesions, which can be cured by hematopoietic stem cell transplantation.
Intestinal IFN-γ<sup>+</sup> T<sub>R</sub>1 cells, but not IL-7 receptor-positive T<sub>H</sub> cells or CD25<sup>+</sup> Treg cells, showed lower IL-10 expression in patients with IBDs.
These data indicate that inflammation-driven colon carcinogenesis in IL10 KO mice and IBD patients is associated with oxidative DNA damage and overt presence of DSB.<i></i>.
Additionally, clinical experience using interleukin 10-secreting <i>Lc. lactis</i> has been shown to be safe and to facilitate biological containment in IBD therapy.
These results indicate that both the <i>IL-10</i> gene itself, and through epistatic interaction with genes within the IL-10/STAT3 signaling pathway, contribute to the risk of pediatric IBD.
We describe a child presenting with intractable bloody diarrhoea since 2 weeks of age and with severe nappy ulceration, who was ultimately diagnosed as having inflammatory bowel disease (IBD) due to an immunodeficiency in the IL-10 receptor.
The present study was designed to investigate the possible association between polymorphisms within Interleukin IL-4 and IL-10 genes and susceptibility to and clinical features of IBD.
While specific mutations in interleukin 10 (IL-10), the IL-10 receptor (IL-10R), and mutations in NCF2, XIAP, LRBA, and TTC7 have been identified in VEO-IBD, polymorphisms in these genes are also associated with increased risk of developing IBD in adolescence or adulthood.
Double IL-10<sup>eGFP</sup> Foxp3<sup>mRFP</sup> reporter mice and transgenic mice with impairment in IL-10 receptor signaling were used to test the activity of T<sub>R</sub>1 cells in a murine inflammatory bowel disease model, a model that resembles the trials performed in humans.
Job's (hyper IgE) syndrome or inflammatory bowel disease (IBD) have now established a clear-cut role for the IL-10/STAT3 axis in immune tolerance; further understanding of these processes could lead to novel therapeutic approaches for autoimmune diseases.