If intestinal microbial involvement has been documented so far in many pathologies that affect a large part of the global population, the protective role of intestinal microbiota in the development of type I diabetes is now confirmed by a series of research that opens new therapeutic opportunities.
We already know that the human intestines host billions of bacteria that form an ecosystem called the microbiota, which is unique to each individual. A team of researchers went further, and demonstrated the protective role of microbiota in the development of type I diabetes in vivo, in laboratory mice.
Type I diabetes is an autoimmune disease where certain cells in the immune system attack the beta cells of the insulin-producing pancreas, the vital hormone that regulates blood glucose. These cells are destroyed if they are recognized by the immune system as "non self". Therefore, the researchers assume that there is a substance that protects beta cells in healthy people.
A research team coordinated by Julien Diana, a researcher at INSERM 1 (National Institute of Santé et Recherche Médicale), dealt with the analysis of catelicidine molecules, antimicrobial peptides known to regulate the immune system in autoimmune diseases. These catechidines may interfere with the control of type 1 diabetes.
The researchers used two types of laboratory mice: one healthy and one diabetic. They have observed that pancreatic cells of healthy mice produce catechidines, while, in diabetic mice, they are produced in a small amount. To test their hypothesis, researchers injected antimicrobial peptides in ill mice. "Cedicillin injection controls inflammation in the pancreas and therefore controls the development of autoimmune diabetes in these laboratory animals.”, the authors of the study said.
The synthesis of catelicidins is stimulated by short-chain fatty acids produced by bacteria in the microbiota. Low production of these peptides in diabetic mice may be associated with an imbalance of the intestinal flora. Experiments confirmed that, compared to health ones, ill mice exhibit a short chain fatty acid deficiency. Transferring a sample of the healthy mice microbiota to the diseased mice resulted in the restoration of a normal level of catelicidine in these laboratory mice. Also, the incidence of diabetes decreased.
"This research is further evidence of the indisputable role of the microbiota in autoimmune diseases and, in particular, of how the development of autoimmune diabetes may be controlled”, the authors of the study said.
According to specialty literature, a similar mechanism exists in humans. If this is confirmed in future studies, it may pave the way for new therapies in diabetes from the point of view of effective modulation of the intestinal microbiome and a corresponding bifidogenic effect.