The Immunomodulatory Effect of the Gut Microbiota in Kidney Disease

Figure 2

Correlation between intestinal microbiota and the incidence of lupus nephritis. Under the symbiotic condition, intestinal microorganisms can affect gut tolerance, immunity, and sensitivity to inflammation through B cell maturation, Treg/Th17 ratio balance, and anti-inflammatory cytokine secretion. In SLE patients, the intestinal inflammatory atmosphere can induce B cells to release autoantibodies, resulting in an imbalance of the Treg/Th17 ratio, leading to intestinal tolerance disorders, beyond immune response and autoimmunity, and tissue/organ damage (such as lupus arthritis (LN)). A large number of autoantibodies and immune complexes are produced and enter the circulation. The deposition of autoantibodies and immune complexes in the glomeruli leads to the activation of complement components (e.g., C3a and C5), resulting in the endothelial cell or podocyte injury and recruitment of immune cells. Infiltrated Th17 cells in the kidney secrete cytokines IL-17A and IL-17F, which activate mesangial cells and tubular epithelial cells to produce CXCL5 and CCL20, then recruit more Th17 cells and neutrophils through CCR6 and CXCR2, respectively. At the same time, ROS produced by infiltration of immune cells can lead to further renal inflammation and tissue destruction.