Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that was traditionally thought to be closely related to genetic and environmental risk factors. Although treatment options for SLE with hormones, immunosuppressants, and biologic drugs are now available, the rates of clinical response and functional remission of these drugs are still not satisfactory. Currently, emerging evidence suggests that gut microbiota dysbiosis may play crucial roles in the occurrence and development of SLE, and manipulation of targeting the gut microbiota holds great promises for the successful treatment of SLE. The possible mechanisms of gut microbiota dysbiosis in SLE have not yet been well identified to date, although they may include molecular mimicry, impaired intestinal barrier function and leaky gut, bacterial biofilms, intestinal specific pathogen infection, gender bias, intestinal epithelial cells autophagy, and extracellular vesicles and microRNAs. Potential therapies for modulating gut microbiota in SLE include oral antibiotic therapy, fecal microbiota transplantation, glucocorticoid therapy, regulation of intestinal epithelial cells autophagy, extracellular vesicle-derived miRNA therapy, mesenchymal stem cell therapy, and vaccination. This review summarizes novel insights into the mechanisms of microbiota dysbiosis in SLE and promising therapeutic strategies, which may help improve our understanding of the pathogenesis of SLE and provide novel therapies for SLE.
Highlights
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the generation of autoantibodies and immune complexes, which can cause multiple organ damage to the skin, kidney, and central nervous system [1]
It follows that the reduced F/B ratio is an important manifestation of gut microbiota dysbiosis in patients with SLE
Previous studies have shown that high-salt diet (HSD) could activate dendritic cells (DCs) and induce the production of pathogenic T Helper 17 (Th17) cells through the p38/MAPK-STAT1 signaling pathway, resulting in gut microbiota dysbiosis, hypertension and autoimmune progression [37,38,39]
Summary
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the generation of autoantibodies and immune complexes, which can cause multiple organ damage to the skin, kidney, and central nervous system [1]. Previous studies have shown that the mechanisms associating gut microbiota dysbiosis and SLE pathogenesis include immune system imbalance, molecular mimicry, impaired intestinal barrier function, biofilms, and sex hormones. Previous studies have shown that interventions targeting the gut microbiota for SLE include dietary interventions, probiotics or prebiotics, antibiotic therapy, vaccination, and fecal microbiota transplantation (FMT). These treatments are currently only studied in lupus murine models, and further clinical trials are required to confirm their efficacy.
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