Actuality. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects various organs and systems, including the skin, kidneys, cardiovascular, nervous, digestive, respiratory and other systems. Despite significant progress in the study of pathogenesis, factors affecting the occurrence and exacerbation of SLE remain poorly understood. Recent studies demonstrate the important role of intestinal microbiota in the regulation of immune processes, which opens up new opportunities for understanding the mechanisms of SLE occurrence and the search for potential therapeutic targets [1, 2].
Purpose. Establishing the relationship between dysbiotic changes in the intestine and the occurrence of systemic lupus erythematosus, identifying key microorganisms involved in the pathogenesis of the disease, and analyzing their impact on the immune response regulation.
Materials and methods. The review used scientific articles published in peer-reviewed journals (PubMed, Scopus, Web of Science) over the past 10 years. The main attention was paid to studies that included the analysis of the microbiota of patients with SLE using metagenomic sequencing and experiments on animal models [3, 4].
Research results. Patients with SLE have been shown to have a significant imbalance in the gut microbiota. In particular, studies have shown a decrease in the number of beneficial bacteria: Lactobacillus and Bifidobacterium, which contribute to the maintenance of the intestinal barrier and exhibit anti-inflammatory properties [5, 6]. Increased levels of pathogenic and opportunistic pathogens, such as Ruminococcus gnavus, as well as microorganisms from the genera Enterococcus, Proteobacteria and Clostridium, which can cause intestinal dysfunction and activate inflammatory processes, have been found [3, 7]. At the same time, a correlation with the severity of the disease was found during a literature review: an increased number of R.gnavus is associated with higher titers of antinuclear antibodies and a more severe course of the disease [4].
Intestinal dysbiosis in SLE affects the immune system through several mechanisms: disruption of the intestinal barrier, activation of inflammatory processes, and reduction of short-chain fatty acids (SCFAs). In dysbiosis, the level of beneficial bacteria that contribute to the production of mucus and the strengthening of intestinal epithelial cells decreases. As a result, the permeability of the intestinal wall increases, which facilitates the entry of bacterial metabolites into the bloodstream and stimulates the activity of the immune system [5]. Some bacteria (family Enterobacteriaceae, Ruminococcus gnavus) contain lipopolysaccharides in their cell wall, which activate Toll-like receptors (TLRs) and trigger the production of pro-inflammatory cytokines, such as interleukin-6 and tumor necrosis factor alpha, which are involved in the pathogenesis of SLE [6]. Beneficial bacteria (genus Bacteroides, Faecalibacterium prausnitzii) produce SCFAs, which have anti-inflammatory properties and support regulatory T cells (Treg). In SLE, their level is significantly reduced, which contributes to hyperactivation of the immune system [7].
Studies of systemic lupus erythematosus in mouse models have confirmed the role of the gut microbiota in the pathogenesis of the disease. In particular, transplantation of microbiota from diseased mice to healthy individuals led to the development of an autoimmune response, indicating the influence of the microbiome on the course of SLE [3]. The use of probiotics enriched with bacteria of the genera Lactobacillus and Bifidobacterium reduced the level of inflammatory cytokines and improved clinical symptoms [8].
Conclusion. The intestinal microbiota plays an important role in the pathogenesis of systemic lupus erythematosus. Studies indicate the important role of microorganisms, such as Lactobacillus, Bifidobacterium, Ruminococcus gnavus, Enterobacteriaceae and Faecalibacterium prausnitzii. These microorganisms may influence the onset or course of systemic lupus erythematosus by modulating the immune response, regulating the intestinal barrier and producing inflammatory mediators. Correction of the intestinal microbiota composition may become a promising direction in the treatment of systemic lupus erythematosus, in particular through the use of probiotics, prebiotics and fecal microbiota transplantation.
List of used literature
1. Hevia, A., et al. (2017). "Autoimmunity and the Microbiome: Paradox or Common Ground?" Trends in Immunology, 38(11), 733-743.
2. Zegarra-Ruiz, D. F., et al. (2019). "A Diet-Sensitive Commensal Lactobacillus Strain Mediates TLR7-Dependent Systemic Autoimmunity." Cell Host & Microbe, 25(1), 113-127.
3. Manfredo Vieira, S., et al. (2018). "Translocation of a gut pathobiont drives autoimmunity in mice and humans." Science, 359(6380), 1156-1161.
4. Azzouz, D., et al. (2019). "Lupus nephritis is linked to disease-perturbed gut microbiota and metabolic signatures." Nature Communications, 10(1), 2162.
5. Mu, Q., et al. (2017). "Leaky Gut and Autoimmune Diseases." Frontiers in Immunology, 8, 598.
6. Bellocchi, C., & Volkmann, E. R. (2018). "Update on gut microbiome dysbiosis in systemic sclerosis and systemic lupus erythematosus." Current Rheumatology Reports, 20(8), 49.
7. Li, Y., et al. (2020). "Dysbiosis of gut microbiome in autoimmune diseases." Frontiers in Immunology, 11, 595.
8. Luo, X. M., et al. (2018). "Gut microbiota in lupus: A potential target for therapeutic intervention." Journal of Immunology Research, 2018, 4956295.
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