Salmonella Enteritidis (SE) is a facultative intracellular pathogen that colonizes the chicken gut leading to contamination of carcasses during processing. A reduction in intestinal colonization by SE could result in reduced carcass contamination thereby reducing the risk of illnesses in humans. Short chain fatty acids such as butyrate are microbial metabolites produced in the gut that exert various beneficial effects. However, its effect on SE colonization is not well known. The present study investigated the effect of sub-inhibitory concentrations (SICs) of sodium butyrate on the adhesion and invasion of SE in primary chicken enterocytes and chicken macrophages. In addition, the effect of sodium butyrate on the expression of SE virulence genes and selected inflammatory genes in chicken macrophages challenged with SE were investigated. Based on the growth curve analysis, the two SICs of sodium butyrate that did not reduce SE growth were 22 and 45 mM, respectively. The SICs of sodium butyrate did not affect the viability and proliferation of chicken enterocytes and macrophage cells. The SICs of sodium butyrate reduced SE adhesion by ∼1.7 and 1.8 Log CFU/mL, respectively. The SE invasion was reduced by ∼2 and 2.93 Log CFU/mL, respectively in chicken enterocytes (P < 0.05). Sodium butyrate did not significantly affect the adhesion of SE to chicken macrophages. However, 45 mM sodium butyrate reduced invasion by ∼1.7 Log CFU/mL as compared to control (P < 0.05). Exposure to sodium butyrate did not change the expression of SE genes associated with motility (flgG, prot6E), invasion (invH), type 3 secretion system (sipB, pipB), survival in macrophages (spvB, mgtC), cell wall and membrane integrity (tatA), efflux pump regulator (mrr1) and global virulence regulation (lrp) (P > 0.05). However, a few genes contributing to type-3 secretion system (ssaV, sipA), adherence (sopB), macrophage survival (sodC) and oxidative stress (rpoS) were upregulated by at least twofold. The expression of inflammatory genes (Il1β, Il8, and Mmp9) that are triggered by SE for host colonization was significantly downregulated (at least 25-fold) by sodium butyrate as compared to SE (P < 0.05). The results suggest that sodium butyrate has an anti-inflammatory potential to reduce SE colonization in chickens.

沙门氏菌肠炎沙门氏菌（SE）是一种兼性的细胞内病原体，在鸡肠道内定殖，导致加工过程中contamination体受到污染。SE引起的肠道菌落减少可减少reduced体污染，从而降低人类患病的风险。短链脂肪酸（例如丁酸）是肠道中产生的微生物代谢产物，可发挥多种有益作用。然而，其对SE定殖的作用尚不为人所知。本研究调查了丁酸钠的亚抑制浓度（SICs）对原代鸡肠细胞和鸡巨噬细胞中SE的黏附和侵袭的影响。此外，研究了丁酸钠对SE攻击的鸡巨噬细胞中SE毒力基因和选择的炎症基因表达的影响。根据生长曲线分析，没有降低SE生长的两个丁酸钠SIC分别为22和45 mM。丁酸钠的SIC不会影响鸡肠细胞和巨噬细胞的活力和增殖。丁酸钠的SIC分别使SE附着力降低约1.7和1.8 Log CFU / mL。鸡肠细胞中SE的侵袭分别降低了约2和2.93 Log CFU / mL（P<0.05）。丁酸钠没有显着影响SE对鸡巨噬细胞的粘附。但是，与对照组相比，45 mM丁酸钠可将浸润降低约1.7 Log CFU / mL（P<0.05）。暴露于丁酸钠并没有改变与运动相关的SE基因的表达（flgG，prot6E），入侵（v），类型3分泌系统（sipB， 点子），在巨噬细胞（病毒， 镁碳），细胞壁和膜的完整性（塔塔），外排泵调节器（1号）和全球毒力法规（lrp） （P> 0.05）。但是，一些基因有助于3型分泌系统（病毒， 西帕），遵守情况（B），巨噬细胞的生存（超氧化物歧化酶）和氧化应激（服务）至少上调了两倍。炎症基因的表达（1号β， 8号和 mp9与SE相比，丁酸钠将SE触发的宿主定植显着下调（至少25倍）P<0.05）。结果表明，丁酸钠具有消炎作用，可减少鸡的SE定殖。