Involvement of Gut Microbiota in SLE and Lupus Nephritis

Abstract

Lupus nephritis is a severe manifestation of systemic lupus erythematosus (SLE). It is caused by immune dysregulation and kidney inflammation. In recent findings, gut microbiota potentially acts as primary mediators to enhance immune complex deposition, complement activation, and macrophage infiltration, and led to renal inflammation. Gut inflammation, known as leaky gut, allows pathogenic bacteria to enter the blood stream to form immune complexes which deposit on the kidney. Lymphocytes and macrophages induct a proinflammatory cytokine milieu that leads to kidney inflammation. Accumulating pieces of evidence from the field of gender bias, dietary habit, alcohol, smoking and antibiotic consumption were closely related to dysbiosis of gut microbiota in SLE. However, little is known about the causes of gut microbiota dysbiosis and the potential pathway that leads to lupus nephritis (LN) flare. In this review, we will bring into deeper insight for the potential link of gut microbiota on immune system with a particular focus on renal inflammation. Moreover, we also discuss the potential novel therapies that regulate gut composition to improve or complement the current treatment of LN.

Keywords: SLE; gut microbiota; leaky gut; lupus nephritis; probiotic.

Figure 1

Summary of defective barrier function caused by gut dysbiosis that promote to lupus nephritis. IAP: intestinal alkaline phosphatase, LPS: lipopolysaccharides, TJ: tight junction, IL: interleukin, TNF: tumor necrosis factor, IFN: interferon, NF-κB: nuclear factor kappa beta, TLR: toll-like receptor, IC: immune complexes, : Increment.