Although DSS and TNBS are widely acknowledged to more effectively mimic IBD’s chronic inflammation and intestinal epithelial destruction features while activating multiple immune pathways [107,108,109], LPS—as a principal component of Gram-negative bacterial outer membranes—primarily mediates signaling through TLR4 receptor binding and the MyD88/NF-κB pathway, rendering it more suitable for studying bacterial infection-associated acute inflammation while being unable to replicate chronic intestinal inflammation’s comprehensive pathological process fully. The gene discussed is MYD88; the disease is bacterial infectious disease.