The ability to prevent or reverse autoimmune diabetes in laboratory animals such as the NOD mouse and BB rat using different therapeutic approaches has initiated several prevention and intervention studies in humans. Delli, Åke Lernmark, in Endocrinology: Adult and Pediatric (Seventh Edition), 2016 Prevention Interestingly, the release of IL-17 was markedly reduced in CD4 T cells from diseased Ramp1-deficient mice suggesting that CGRP enhances the development of experimental allergic encephalomyelitis by promoting IL-17 production.Īhmed J. Th17 cells are considered important for induction of this autoimmune disease ( Bettelli et al., 2007 Ouyang et al., 2008). Ramp1-deficient mice show an attenuated development of experimental allergic encephalomyelitis after immunization with myelin oligodendrocyte glycoprotein peptide ( Mikami et al., 2012). However, in this model, the systemic release of CGRP was found to alter splenic T cell responses leading to impaired proliferation and IFNγ production, and to an increased release of IL-10. Similarly, CGRP gene transfer decreased the morbidity of diabetes caused by multiple injections of low-dose streptozocin and inhibited lymphocyte infiltration into the islets ( Sun et al., 2003). Local production of CGRP markedly reduced the incidence of diabetes and the development of peri-insulitis, but did not lead to systemic effects. The functions of CGRP in autoimmune diabetes were studied in NOD mice with transgenic expression of CGRP in pancreatic β cells ( Khachatryan et al., 1997). īernhard Holzmann, in Encyclopedia of Immunobiology, 2016 Autoimmune Diseases Bacteriotherapy is a potential tool to modulate the immune system in the prevention of islet cell autoimmunity. Beneficial effects of Lactobacillus rhamnosus and Bifidobacterium lactis on β-cell function would create a rationale for its use in patients with newly diagnosed T1D. Lactobacillus and Bifidobacterium are important genera in the colon microbiota of humans. In humans, early probiotic administration could decrease the risk of islet autoimmune reactions in children, with high genetic risk to develop the disease. Probiotic supplementation has been hypothesized to affect innate and adaptive immune responses to environmental antigens by supporting healthy gut microbiota, and could therefore be used to prevent the onset of T1D-associated islet autoimmunity and treat the established disease. Additionally, probiotic supplementation increased the Firmicutes/Bacteroidetes ratio, Clostridium species, and butyrate-producing bacteria in the gut. These beneficial effects could involve the migration of intestinal Treg cells to the pancreatic lymph nodes, and alterations in the Th1/Th2/Th17 balance, favoring an antiinflammatory milieu in the gut and pancreas. Insulitis was suppressed, disease onset was delayed, and glucose metabolism improved. The administration of probiotic Clostridium butyricum induces Treg cells in the pancreas, and consequently inhibits the diabetes onset in NOD mice. However, Lactobacillaceae-enriched probiotic in NOD mice poorly colonized the intestine and were insufficient to overcome the effects of a diabetogenic microbiome. Diabetes susceptibility correlated with reduced fecal SCFAs. Somewhat conflicting experimental results are announced as well. Moreover, antibiotic exposure accelerated diabetes onset in NOD mice, accompanied by increased Th1 and Th17 cells in the mucosal-associated lymphoid tissues. Fecal transplantation of NOD microbes induced insulitis in NOR hosts, suggesting that the NOD microbiome is diabetogenic. The intestinal microbiota from NOD mice housed more pathobionts and fewer beneficial microbes. įecal transplantation between NOD and resistant NOD mice (NOR) and oral antibiotic and probiotic treatment of NOD mice modulate pancreatic function. In addition, treated NOD mice showed modulation of the gut immunity by induction of CD103 dendritic cell differentiation and suppression of Th1 and Th17 subsets in the gut mucosa. Likewise, the administration of Lactobacillaceae-enriched probiotic alone or in combination with retinoic acid protected NOD mice from diabetes by suppressing inflammasome activation, IL-1β expression, and by inducing the immunomodulatory indoleamine 2,3-dioxygenase and IL-33 secretion. The protective effect was transferable to irradiated mice receiving diabetogenic cells and splenocytes from treated mice. This protection was associated with increased IL-10 secretion in Peyer patches, spleen, and pancreas. Gislane Lellis Vilela de Oliveira, in Microbiome and Metabolome in Diagnosis, Therapy, and other Strategic Applications, 2019 Probiotics in T1DĮarly oral administration of Lactobacillaceae -enriched probiotic prevented diabetes in NOD mice by abrogating insulitis and β-cell destruction.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |