Salmonella enterica serovar Typhimurium (S. Typhimurium) continues to be a serious concern to the poultry industry as a bacterial foodborne zoonosis, which generally results in intestinal inflammation and barrier dysfunction or even death. Eugenol is a phenolic compound with various pharmacological activities involved antioxidant, anti-inflammatory, and antibacterial effects, which is expected to be an effective nonantibiotic therapy. The purpose of this study was to explore the protective effects of eugenol in the cellular and broiler models of S. Typhimurium infection and the possible underlying mechanisms. The results of animal infection showed that eugenol treatments enhanced the relative weight gains and survival rates of broilers with a reduction of the organ bacterial load and intestinal ultrastructural injury. Moreover, eugenol significantly inhibited the mRNA levels of myeloid differentiation factor 88 (MyD88) and toll-like receptor-4 (TLR4), then declined the phosphorylation of p65 and IκBα of NF-κB pathway and the expressions of inflammatory factors (TNF-α, IL-1β, IL-2, and IL-18) in duodenum tissues, while maintained the expressions of intestinal tight junction proteins (ZO-1, claudin-1, occludin). Further experiments in vitro revealed that eugenol markedly inhibited the adhesion and invasion of S. Typhimurium to RAW264.7 or IEC-6 cells, then reduce bacterial multiplication in IEC-6 or DF-1 cells. In conclusion, eugenol could defend broilers from S. Typhimurium infection by stabilizing the intestinal mucosal barrier and relieving inflammatory response, as well as inhibiting bacterial adhesion and invasion to cells.
Keywords: Salmonella Typhimurium; broiler; eugenol; inflammatory response; intestinal tight junction.
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