More than 50 percent of our immune system is found in our digestive tract, which is why it is important to have a properly functioning digestive system.
“Over 500 species of microbes are known to reside in the human gastrointestinal tract (1,2). Their interaction with the mucosal immune system, especially in the first years of life, may have life-long effects. As but one example, differences in the composition of intestinal microflora between healthy and allergic infants in countries with a high and low prevalence of allergies have been noted and precede clinical symptoms (12). Furthermore, probiotics have been successfully used as immunomodulators in the prevention and treatment of allergies in children (13,14), findings indicating that commensal bacteria are not innocent bystanders in humans but active players in the shaping of the immunological network of the host. Hence, new approaches for evaluating the interactions between the intestinal microbiota and barrier and innate immunity are needed.”
“The observation, if confirmed, suggests that either chronic enterovirus infection in type 1 diabetes or predisposition to recurrent enterovirus infections, rather than accidental role of enterovirus infections, is responsible for the induction of β-cell autoimmunity. Indeed, enteral infections are known to change the cytokine pattern (44) and increase the permeability of the gut (45), which in some cases may lead to enhanced immunity to food proteins. ”
“Dietary factors, especially those during infancy when new foreign proteins are introduced into the diet, modulate the intestinal microbiota (50). In NOD mice, diabetes-preventive gluten free–diet has been shown to modulate microbiota (51). It is notable that dietary interventions may thus not only modulate the immune response to dietary exposure but also immunity in general by changes in microbiota and permeability. The interaction of tolerance, microflora, and permeability was demonstrated when probiotics given to children with atopic dermatitis resulted in a decrease of the intestinal permeability and alleviated the symptoms of dermatitis (52).”
“The lymphocytes from intestine may therefore circulate between the pancreas and gut, or dendritic cells may transport luminal antigens for presentation in the pancreatic lymph nodes. These findings provide an immunological link between dietary antigens and insulitis, which has been earlier observed as modulation of diabetes outcome by dietary manipulation in animal models. The Trial to Reduce IDDM in the Genetically at Risk (TRIGR) study is currently testing the elimination of cow milk proteins and the use of hydrolyzed formula during the first months of life in children at genetic risk of type 1 diabetes for the purpose of preventing β-cell autoimmunity. The trial is based on encouraging results from a pilot study in which a 50% reduction of the β-cell autoimmunity was observed in children who received hydrolyzed formula versus those who received ordinary cow milk–based formula (57). This intervention may have multiple actions that modulate the development of β-cell autoantibodies. The intervention may alter the composition of intestinal microbiota, promote tolerance by diminishing intestinal permeability and inflammation, or modulate immune response to bovine insulin by delaying exposure until the time of normal intestinal maturation.”
“Finally, the role of gut as modulator of β-cell autoimmunity, and/or as the place for initiation of β-cell autoimmunity, should provide new understanding of the changing incidence of type 1 diabetes at different times and in different populations.”