It has been long recognized that a bidirectional relationship between the brain and intestine exists
[9]. A good example is multiple sclerosis (prevalence 150 per 100,000 subjects with more females than
males affected, age of onset 20–40 years), an autoimmune chronic inflammatory disease associated with
degradation of fatty myelin sheaths around the axons of the brain and spinal cord, resulting in neurologic
debilitating symptoms [10]. Recent studies have identified a crucial role for intestinal bacteria species
which via an IL-17-dependent process are able to trigger autoimmune-mediated demyelination [1
1].
Although no studies are yet available on the intestinal microbiota composition in patients with multiple
sclerosis, it is known that these subjects are characterized by an increased intestinal permeability [12],
thus facilitating bacterial translocation fromthe intestine into the bloodstream. Albeit in a small group of