NFKB1 and bacterial urinary tract infection: Cui et al.12 confirmed that IL-1β, TNF-α and NF-κB activities were inhibited by UTI treatment in TBI, which resulted in intracellular ROS accumulation and decrease TLR4 expression levels, and the TLR4/NF-kB/p65 signalling pathway also directly regulates oxidative stress and apoptosis.