SummaryIn humans, a complex interaction between the host immune system and commensal microbiota is required to maintain gut homeostasis. In this symbiotic relationship, the microbiota provides carbohydrate fermentation and digestion, vitamin synthesis and gut-associated lymphoid tissue development, as well as preventing colonization by pathobionts, whereas the host offers a niche and nutrients for the survival of the microbiota. However, when this mutualistic relationship is compromised and an altered interaction between immune cells and microorganisms occurs, the gut microbiota may cause or contribute to the establishment of infectious diseases and trigger autoimmune diseases. Researchers have made efforts to clarify the role of the microbiota in autoimmune disease development and find new therapeutic approaches to treat immune-mediated diseases. However, the exact mechanisms involved in the dysbiosis and breakdown of the gut epithelial barrier are currently unknown. Here, we provide a general overview of studies describing gut microbiota perturbations in animal models of autoimmune diseases, such as type 1 diabetes, multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus. Moreover, we include the main studies concerning dysbiosis in humans and a critical discussion of the existing data on the use of probiotics in these autoimmune diseases.

Intestinal dysbiosis associated with immunological deregulation, leaky gut, bacterial translocation, and systemic inflammation has been associated with autoimmune diseases, such as type 1 diabetes (T1D). The aim of this study was to investigate the intestinal dysbiosis in T1D patients and correlate these results with clinical parameters and cytokines. The present study was approved by the Barretos Cancer Hospital (Process number 903/2014), and all participants have signed the informed consent in accordance with the Declaration of Helsinki, and answered a questionnaire about dietary habits. Stool samples were used for bacterial 16S sequencing by MiSeq Illumina platform. IL-2, IL-4, IL-6, IL-10, IL-17A, TNF, and IFN-γ plasma concentrations were determined by cytometric bead arrays. The Pearson’s chi-square, Mann–Whitney and Spearman correlation were used for statistical analyses. Alpha and beta diversities were conducted by using an annotated observed taxonomic units table. This study included 20 patients and 28 controls, and we found significant differences (P < 0.05) among consumption of vegetables, proteins, milk and derivatives, spicy food, and canned food when we compare patients and controls. We detected intestinal dysbiosis in T1D patients when we performed the beta diversity analysis (P = 0.01). The prevalent species found in patients’ stool were the Gram-negatives Bacteroides vulgatus, Bacteroides rodentium, Prevotella copri, and Bacteroides xylanisolvens. The inflammatory interleukin-6 was significantly increased (P = 0.017) in patients’ plasma. Furthermore, we showed correlation among patients with poor glycemic control, represented by high levels of HbA1C percentages and Bacteroidetes, Lactobacillales, and Bacteroides dorei relative abundances. We concluded that there are different gut microbiota profiles between T1D patients and healthy controls. The prevalent Gram-negative species in T1D patients could be involved in the leaky gut, bacterial translocation, and poor glycemic control. However, additional studies, with larger cohorts, are required to determine a “signature” of the intestinal microbiota in T1D patients in the Brazilian population.