Additionally, in the ΔfliC infection group, pro-inflammatory genes (such as Tlr5, Tnfα, and Il1β) were downregulated, while lipid metabolism-related genes (such as Acox1, Cpt1a, and Pparα) were upregulated, suggesting the suppression of the Tlr5/NF-κB immune signaling axis and enhanced fatty acid β-oxidation. The gene discussed is TNF; the disease is infection.