The interplay between the gut microbiota and the immune system in the mechanism of type 1 diabetes.

PURPOSE OF REVIEW

Discuss recent data linking the intestinal microbiome with mechanisms of inflammation and islet destruction.

RECENT FINDINGS

Type 1 diabetes (T1D) is a proinflammatory disease that results in the loss of insulin-producing beta cells. How T1D is triggered is unclear; however, both genetic and environmental factors were implicated in disease mechanisms. Emerging evidence supports the notion that there is a complex interaction between the intestinal microbiome and the immune system and this cross-talk is involved in maintaining normal immune homeostasis in the gut and periphery. Under some circumstances the gut microbiota could lead to pathogenic immune responses resulting in inflammation in the intestine as well as other organs. Indeed, recent data from genetically susceptible individuals suggested that alterations in gut bacterial communities may be involved in the mechanism of islet destruction. Studies performed in animal models of T1D indicated that manipulating the gut microbiome can protect from islet destruction via mechanisms that may involve down-regulating both the adaptive and innate immune systems.

SUMMARY

Further work is required to identify specific bacterial communities and mechanisms involved in triggering T1D. A better knowledge of the role of the gut microbiome in islet destruction could lead to new clinical interventions to restore healthy homeostasis and prevent disease development.