The damage was further exacerbated by a decrease in IL-18, an interleukin responsible for antiapoptosis and mucosal restitution.49,50 At this point, it is noteworthy that AMPs like RegIII and sPLA2 also have TLRs-mediated pro-inflammatory properties.48 It was speculated that mediated by SaaS, Salmonella affected TLR 4/5 levels and then regulate RegIIIβ/γ secretion, thereby modulating the inflammatory response and compromising the innate defense.51 Decreased expression of Cldn at 72 hpi in this work was also confirmed by studies involving conventional intestine infections with Salmonella. The gene discussed is IL18; the disease is digestive system infectious disorder.