Right from the get-go, this study peaked my interest. In this experimental model of multiple sclerosis, healthy mice are inoculated with a chemical called
myelin oligodendrocyte glycoprotein. It takes them 2 weeks to fully develop experimental autoimmune encephalomyelitis (EAE) and only about 80% of the mice do develop the disease. The animals that are going to develop EAE characteristically lose weight, about 10% of their body weight, about 1 week after the inoculation (they typically start to show symptoms about 8-10 days after with full development of the disease at the 2-week mark).
What the researchers did was to select those animals who were developing EAE based on whether or not they lost weight at the 1-week mark. Then, they measured intestinal permeability (whether or not the gut is leaky) at 1 week (before development of the disease) and at 2 weeks (after the disease had fully developed). What they found was that a leaky gut was present at 1 week, before the disease fully develops. A leaky gut comes first.
The researchers further characterized exactly what type of damage was being done to the gut to make it leaky as well as exactly how the immune system was being stimulated in the gut. The same types of immune system cells known to be culprits in the damage to the myelin sheath in EAE were accumulating in the tissues of the gut and causing damage there too. And regulatory T-cells, which are supposed to reign in the immune system but are deficient in autoimmune disease, were low in the intestine. Even more interesting, the protein zonulin, which has been implicated as the protein stimulated by gluten that causes a leaky gut via direct action on the tight junctions in celiac disease, was increased (again, lots more details on the effects of zonulin and the roles of different immune cell types in autoimmune disease can be found in
The Paleo Approach). Taken together, this all looks very much like a gut being attacked by a dysfunctional immune system.
