Existing studies have shown that B. producta can exert intestinal protective effects through multiple mechanisms: including directly inhibiting excessive inflammatory responses, enhancing intestinal mucosal barrier function, regulating pro-inflammatory signaling pathways such as TLR4/NF-κB, and restoring the ecological balance of intestinal microbiota, thereby effectively improving dextran sulfate sodium (DSS)-induced experimental colitis (Mao et al., 2024). The gene discussed is TLR4; the disease is colitis.