Type 1 diabetes (T1D) scientists have believed for some time that communities of bacterial microorganisms in the gut, which make up the microbiome, are in some way related to immune system defects and the autoimmune response that leads to T1D. Previous research has hypothesized that the diversity or abundance of specific bacteria within the microbiome plays a critical role in shaping our immune system. However, a new JDRF-funded study published in March paints a different picture that may give researchers an eye-opening foundation from which to base future studies—and from which we may begin to better understand the relationship between autoimmunity and the gut. Researchers from the Institute of Diabetes Research, Helmholtz Zentrum Munchen, Germany and the University of Florida, Gainesville studied the gut microbiomes of 44 children from infancy to age three (from the JDRF-funded BABYDIET study). They found that in the group of children with anti-islet autoantibodies, who subsequently developed T1D, certain bacteria within the gut microbiome were for some reason more physically isolated from other bacterial species. These bacteria did not display the normal symbiotic interactions that appear to occur in those without anti-islet autoantibodies, and this uncommunicative behavior occurred regardless of bacterial abundance or diversity within the gut microbiome. Researchers believe that the lack of sufficient bacterial integration and subsequent breakdown in communication within the gut microbiome may combine with certain environmental triggers to contribute to the pathogenesis of T1D. Such triggers could include complex interactions between factors such as method of birth, genetics, and nutrition of both mother and baby—all of which are known to affect the gut microbiome. Future research is now needed to include study participants without a familial predisposition to T1D, to explore the possible causes of the interesting bacterial interplay revealed in this latest study, and to discover how these findings are related to the immune system defects and autoimmunity associated with T1D. These next stages in research could help lead to novel prevention therapies for people at risk of developing the disease.
Enteroviruses have been connected to T1D in various studies. A new JDRF-funded study published in February 2014 evaluated the association between specific types of enteroviruses and T1D by measuring type specific antibodies against the group B coxsackieviruses (CVBs, a type of enterovirus), which have been linked to T1D in previous surveys. Altogether, 249 children with newly diagnosed T1D and 249 control children matched according to sampling time, sex, age, and country were recruited in Finland, Sweden, England, France, and Greece between 2001 and 2005 (mean age 9 years). Antibodies against CVB1 (a specific coxsackieviruses) were more frequent among diabetic children than among control children, whereas other CVB types did not differ between the groups. CVB1- associated risk was not related to T1D genotype, age, or sex. The results support previous studies that suggested an association between CVBs and T1D, highlighting the possible role of CVB1 as a T1D causing virus type. If a causal link can be confirmed, vaccines against these enteroviruses could be developed as a prevention therapy.