IL1B and escherichia coli infection: After E. coli infection, NF-κB is activated, and these pro-inflammatory factors such as interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α lead TJ damage (13), while NF-κB activates myosin light chain kinase (MLCK) and then activates myosin light chain (MLC) (13), which makes IL-1β and TNF-α levels increased, and caused the contraction of peri-junctional actin-myosin filaments and opening of the barrier (14).