Lupus Nephritis and Dysbiosis

Abstract

Lupus nephritis (LN) is one of the most common and serious complications of systemic lupus erythematosus (SLE). The risk factors for developing LN by SLE patients are not fully understood. They are considered to be a mix of genetic and environmental variables, one of them being dysbiosis, proposed recently to interfere with autoimmunity. As of yet, the relations between the human microbiome, its genetic determinants, individual variability and clinical consequences remain to be established. One of the major obstacles in studying them is the magnitude of confounders, such as diet, drugs, infections or antibiotics use. They also make comparison between the studies extremely complicated. We reviewed the available evidence for the interplay between microbiome, dysbiosis and mechanisms triggering the autoimmune responses and potentially contributing to LN development. One such mechanism is the stimulation of autoimmune responses by bacterial metabolites that can mimic autoantigens and cause antibody production. These mimicking microbial antigens seem to be a promising target for future interventions.

The Disease with a Thousand Faces and the Human Microbiome—A Physiopathogenic Intercorrelation in Pediatric Practice

“…Regarding the clinical picture of subjects with SLE, Visitación N. et al postulate, through the study of changes in the cardiovascular system in relation to the intestinal microbiota in murine models, the link between this and the development of endothelial dysfunction, vascular inflammation and hypertension [92]. Lupus nephritis, one of the frequent and feared complications of SLE, seems to have part of its origin in the alteration of intestinal permeability (in addition to aspects such as genetic factors and the individual characteristics of the subject), an aspect that leads over time to the potentiation of autoimmune responses due to metabolites of bacteria that mimic autoantigens, leading to chronic inflammation mediated by lymphocytes and macrophages, activation of the complement and its deposition at the renal level, with intestinal dysbiosis thus becoming one of the possible targets in nephropathy therapy [93,94].…”