Type 1 diabetes is commonly found in young children and adults. It is an autoimmune disease, meaning that our immune system identifies and attacks our organ as a foreign infected unit. A model (shown on the left) of the disease development has been proposed. In the model, an unknown stimulant triggers the expansion of immune B-cells and T-cells which causes inflammation and destruction of cells within the pancreatic islet. The pancreatic islet contains hormone-producing endocrine cells, such as beta cells. The beta cells are responsible in producing insulin that distributes glucose from blood to tissues. As a result of the B- and T-cells expansion, destruction of beta cells disables the production of insulin. The reduction of insulin causes a high level of glucose remained in the bloodstream. This hyperglycemia state (high glucose in the bloodstream) is known as Type 1 diabetes.
Toll like receptor is a protein that sits on the surface of cell (in most cases) to detect foreign particles that come off from bacteria or viruses. When it is activated, the signal is relayed to MyD88 in the cytoplasm (shown on right), which then indirectly activates the production of inflammatory proteins. It is recently discovered that if you take out MyD88 gene from diabetic mice, mice no longer have symptoms of diabetes. This protection appears to involve in the change of bacterial composition inside the mice without MyD88 gene. Surprisingly, if you eliminate some bacteria from the intestines in the diabetic mice (without MyD88) by antibiotic treatment, 40% of the mice tested have symptoms of diabetes. And if you eliminate all bacteria from the intestines in the diabetic mice (without MyD88), about 85% of the diabetic mice have symptoms of diabetes in 30 days. So what if you expose this germ free mice (without MyD88) with bacteria? Exposing germ free mice with bacteria reduce inflammation in the pancreatic islet, indicating that intestinal commensal bacteria prevent diabetic mice from Type 1 diabetes.
Complexity of the immune system: changes soldiers to fight
So is it possible to transplant bacteria to Type 1 diabetes patients as a cure? Quite possibly. Fecal bacteriotherapy transplantation has already been used to treat c. difficile infection. This procedure transplants the bacteria in the fecal matter from a healthy individual into the sick individual. This is thought to restore the disrupted bacterial community in the sick individual. Restoring microbiota can be a cure for autoimmune diseases, but for now, this technique has yet fully incorporated into clinical practices.
Here is an idea, there is sperm bank and egg bank out there these days. Why don’t we have a bank that stores all the fecal bacteria when we are healthy? If we get sick, we can go to the bank and restore our normal bacteria.
The “Perfect Storm” for Type 1 Diabetes. The Complex Interplay Between Intestinal Microbiota, Gut Permeability, and Mucosal Immunity. doi: 10.2337/db08-0331 Diabetes October 2008 vol. 57 no. 10 2555-2562
Wen L, Ley RE, Volchkov PY, Stranges PB, Avanesyan L, Stonebraker AC, Hu C, Wong FS, Szot GL, Bluestone JA, Gordon JI, Chervonsky AV.Wen L, Ley RE, Volchkov PY, Stranges PB, Avanesyan L, Stonebraker AC, Hu C, Wong FS, Szot GL, Bluestone JA, Gordon JI, Chervonsky AV. Innate immunity and intestinal microbiota in the development of Type 1 diabetes. Nature. 2008 Oct 23;455(7216):1109-13. Epub 2008 Sep 21.