In the study conducted using non-obese diabetic (NOD) mice, the researchers found that the common stomach bacteria influenced the overly robust immune system responses responsible for the disease.
Previous studies have already shown that NOD mice exposed to killed or non-active strains of tuberculosis or other disease-causing bacteria were protected against Type I diabetes, suggesting that the rapid "innate" immune response that normally protects from infections can significantly affect the onset of Type 1 diabetes.
The current study showed that the NOD mice deficient in innate immunity were protected from diabetes in normal conditions.
Lead researchers Li Wen, at Yale, and Alexander V. Chervonsky, at the University of Chicago, raised the mice in a germ-free environment, lacking "friendly'' gut bacteria.
The results showed that mice lacking the 'good' bacteria found in human intestine developed severe diabetes.
"Understanding how gut bacteria work on the immune system to influence whether diabetes and other autoimmune diseases occurs is very important," Nature magazine quoted Li as saying.
"This understanding may allow us to design ways to target the immune system through altering the balance of friendly gut bacteria and protect against diabetes," Li added.
The study appears in journal Nature.