Dysbiosis of the intestinal microbiota affecting the gut barrier could be triggering Type 1 Diabetes (T1D), the second most frequent autoimmune disease in childhood. This study compared the structure of the fecal microbiota in 29 mestizo children aged 7–18 years, including 8 T1D at onset, 13 T1D after 2 years treatment, and 8 healthy controls. Clinical information was collected, predisposing haplotypes were determined; the fecal DNA was extracted, the V4 region of the 16S rRNA gene amplified and 454-pyrosequenced. The newly diagnosed T1D cases had high levels of the genus Bacteroides (p < 0.004), whereas the control group had a gut microbiota dominated by Prevotella. Children with T1D treated for ≥2 years had levels of Bacteroides and Prevotella compared to those of the control group. The gut microbiota of newly diagnosed T1D cases is altered, but whether it is involved in disease causation or is a consequence of host selection remains unclear.

Type 1 diabetes (T1D) is the second most frequent autoimmune disease in childhood. The long-term micro- and macro-vascular complications of diabetes are associated with the leading causes of disability and even mortality in young adults. Understanding the T1D etiology will allow the design of preventive strategies to avoid or delay the T1D onset and to help to maintain control after developing. T1D development involves genetic and environmental factors, such as birth delivery mode, use of antibiotics, and diet. Gut microbiota could be the link between environmental factors, the development of autoimmunity, and T1D. In this review, we will focus on the dietary factor and its relationship with the gut microbiota in the complex process involved in autoimmunity and T1D. The molecular mechanisms involved will also be addressed, and finally, evidence-based strategies for potential primary and secondary prevention of T1D will be discussed.

Background Intestinal bacterial dysbiosis and increased gut permeability are associated with higher risk of developing type 1 diabetes (T1D) or celiac disease (CD). There is a lack of information on parasitism involved in gut disturbance of predisposed children. We evaluated the effect of enteropathogenic parasites ( Cryptosporidium spp., Cyclospora spp. G. lamblia , and Blastocystis spp.) on the bacterial structure of feces from children with autoantibodies for T1D or CD. Participants included 37 children under 18 years of age, from whom stools were analyzed for enteric parasites by qPCR and 22/37 for bacterial profile by sequencing the V3–V4 region of the 16s rRNA gene. Dietary, clinical, and socioeconomic data was recorded. Results Pathogens parasitized 28/37 participants, Cryptosporidium spp. was the most prevalent (62.2%), followed by both Cyclospora cayetanensis and Blastocystis spp (37.8%). There were no dietary differences ( p > 0.05) attributable to parasitism. Co-infected participants with Cryptosporidium and Cyclospora did not differ (p = 0.064) from non-infected participants in bacterial alpha phylogenetic diversity. The same parasites’ co-infection was associated with a decreased abundance of the Ruminococaceae (p = 0.04) and Verrucomicrobioceae families, of the Akkermansia genus (p = 0.009). There was a lower Firmicutes/Bacteroidetes ratio (p = 0.02) in infected than in uninfected participants. Conclusions Cryptosporidium and Cyclospora affected the bacterial structure at family and genus levels, decreasing the ratio between Firmicutes and Bacteroidetes in children with auto-antibodies for T1D or CD, which could increase the risk of illness onset.

Besides autoimmunity, diet appears to have a central role determining the T1D-associated dysbiosis evolution.

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