RIKEN Center for Integrative Medical Sciences, Japan
Title: Impact of gut microbiota on autoimmune diseases
Biography: Dr. Hiroshi Ohno
Along with the westernization of the lifestyle, prevalence rate has been rapidly increasing for some
diseases, including autoimmune diseases such as multiple sclerosis (MS) and type 1 diabetes mellitus (T1D). This is considered to be attributable to environmental factors. A major environmental factor is gut microbiota. Recent progress in the gut microbiota research, mainly with metagenomic analysis, dysbiosis, such as the loss of diversity in gut microbiota, is associated with many of these diseases. By employing germ-free/gnotobiotic mice models with transferring fecal microbiota from disease patients and model mice, disease-associated dysbiosis could reproduce symptoms. On the other hand, healthy fecal microbiota transplantation can cure refractory Clostridium dificile infection. Thus, dysbiosis in gut microbiota is causative role in the pathogenesis of diseases.
MS is a demyelinating disease caused by autoimmunity toward myelin sheath. By using experimental autoimmune encephalomyelitis (EAE) in mice, an animal model of MS, we have found that small intestinal microbiota is critically involved in its pathogenesis. It seems that two distinct bacteria, providing autoantigen mimicry and T-cell adjuvanticity, are responsible for EAE exacerbation.
We are also investigating the role of gut microbiota in T1D, an autoimmune disease destroying insulin-producing pancreatic -cells.. Employing streptozotocin-induced T1D mice model, we have found that Heligmosomoides polygyrus-derived trehalose ameliorates T1D and affects gut microbiota, which could result in the increase in Foxp3+CD8+Treg cells in the spleen. Treharose increases Ruminococcus species in the gut, implicating its involvement in suppressing T1D pathogenesis.