Contributions
Abstract: 163
Type: Oral
Epidemiology suggests that the development of multiple sclerosis (MS) involves two factors: a genetic predisposition as well as non-genetic triggering factors from the environment. While large-scale genome-wide association studies have identified an immense number of risk genes, the question of the actual disease triggers still awaits a conclusive answer. So far, disease triggers were suspected among infective microbes, but none of the proposed organism has stood the test of time. More recently, an unexpected agent has entered the scene, the commensal gut flora. Initially, antibiotic depletion of intestinal bacteria was found to interfere with the experimental induction of autoimmune encephalomyelitis (EAE). This strategy helped identify bacteria species that either promote or lessen the disease. However, EAE induction relied on active immunization using myelin autoantigen emulsified in strong immune adjuvants, an artificial procedure unrelated to spontaneous triggering of human disease. More recently, spontaneously developing EAE models indeed showed that clinical bouts reminiscent of relapsing-remitting MS, critically depend on an intact gut flora. The mechanisms, how gut microbiota stimulate brain autoimmunity, approaches to interfere with disease development, and translation of experimental findings to clinical MS will be the topics of this presentation.
Disclosure: Hartmut Wekerle: nothing to disclose
Abstract: 163
Type: Oral
Epidemiology suggests that the development of multiple sclerosis (MS) involves two factors: a genetic predisposition as well as non-genetic triggering factors from the environment. While large-scale genome-wide association studies have identified an immense number of risk genes, the question of the actual disease triggers still awaits a conclusive answer. So far, disease triggers were suspected among infective microbes, but none of the proposed organism has stood the test of time. More recently, an unexpected agent has entered the scene, the commensal gut flora. Initially, antibiotic depletion of intestinal bacteria was found to interfere with the experimental induction of autoimmune encephalomyelitis (EAE). This strategy helped identify bacteria species that either promote or lessen the disease. However, EAE induction relied on active immunization using myelin autoantigen emulsified in strong immune adjuvants, an artificial procedure unrelated to spontaneous triggering of human disease. More recently, spontaneously developing EAE models indeed showed that clinical bouts reminiscent of relapsing-remitting MS, critically depend on an intact gut flora. The mechanisms, how gut microbiota stimulate brain autoimmunity, approaches to interfere with disease development, and translation of experimental findings to clinical MS will be the topics of this presentation.
Disclosure: Hartmut Wekerle: nothing to disclose