In CKD rats, gut bacteria could activate a T-helper 17 (Th17)/Th1 T-cell response and increase the production of inflammatory cytokines, and LPS could initiate innate immune cells through nuclear factor kappa B (NF-κB) and toll-like receptor 4 (TLR4) pathways, all triggering inflammation and immune response [65]. This evidence concerns the gene TLR4 and chronic kidney disease.