Dysbiosis and probiotic applications in autoimmune diseases

Abstract

Several evidence in animal models and humans pointed to the involvement of oral and intestinal dysbiosis in the development of autoimmune diseases. Dysbiosis is associated with decreased bacterial function and diversity, as well as decreased beneficial microbes, increased pathobionts, impaired barrier function, bacterial translocation, systemic inflammation, and decreased immune regulatory mechanisms in the gut mucosa. The mechanisms proposed to link dysbiosis with autoimmune diseases include molecular mimicry, bystander T-cell activation, T helper cell skewing, epitope spreading, dual T-cell receptors, posttranslational modification of luminal proteins by dysbiotic microbiota, and amplification by inflammatory cytokines. Studies suggest that probiotics influence systemic immune responses, ensure the homeostasis of the healthy microbiota in the intestinal mucosa, and therefore, could be used as adjuvant therapy to treat immune-mediated diseases. The mechanisms to achieve these effects include mucus secretion, antimicrobial peptide production, cross-feeding other resident microbes, production of organic acids and enzymes, gastrointestinal epithelial barrier maintenance, decreasing oxidative stress, competition with pathogens, and finally, modulation of the host immunity. Here, we described several reports concerning dysbiosis and probiotic applications in animal models of autoimmune diseases, human studies, and clinical trials concerning the applicability of probiotics in autoimmune diabetes, autoimmune thyroid diseases, rheumatoid arthritis, systemic lupus erythematosus, and Sjögren syndrome.