Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, College of Animal Science and Technology, College of Veterinary Medicine, Zhejiang Agriculture and Forestry University, Hangzhou 311300, China.
Zhejiang Vegamax Biotechnology Co., Ltd., Huzhou 313300, China.
Poult Sci. 2024 Apr;103(4):103483. doi: 10.1016/j.psj.2024.103483. Epub 2024 Jan 20.
Salmonella infection is a major concern in poultry production which poses potential risks to food safety. Our previous study confirmed that Lactiplantibacillus plantarum (LP) postbiotic exhibited a strong antibacterial capacity on Salmonella in vitro. This study aimed to investigate the beneficial effects and underlying mechanism of LP postbiotic on Salmonella-challenged broilers. A total of 240 one-day-old male yellow-feathered broilers were pretreated with 0.8% deMan Rogosa Sharpe (MRS) medium or 0.8% LP postbiotic (LP cell-free culture supernatant, LPC) in drinking water for 28 d, and then challenged with 1×10 CFU Salmonella enterica serovar Enteritidis (SE). Birds were sacrificed 3 d postinfection. Results showed that LPC maintained the growth performance by increasing body weight (BW), average daily gain (ADG), and average daily feed intake (ADFI) in broilers under SE challenge. LPC significantly attenuated SE-induced intestinal mucosal damage. Specifically, it decreased the intestinal injury score, increased villus length and villus/crypt, regulated the expression of intestinal injury-related genes (Villin, matrix metallopeptidase 3 [MMP3], intestinal fatty acid-binding protein [I-FABP]), and enhanced tight junctions (zona occludens-1 [ZO-1] and Claudin-1). SE infection caused a dramatic inflammatory response, as indicated by the up-regulated concentrations of interleukin (IL)-1β, IL-6, TNF-α, and the downregulation of IL-10, while LPC pretreatment markedly reversed this trend. We then found that LPC inhibited the activation of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome by decreasing the gene expression of Caspase-1, IL-lβ, and IL-18. Furthermore, LPC suppressed NLRP3 inflammasome activation by inhibiting nuclear factor-kappa B (NF-κB) signaling pathway (the reduced levels of toll-like receptor 4 [TLR4], myeloid differentiation factor 88 [MyD88], and NF-κB). Finally, our results showed that LPC regulated gut microbiota by enhancing the percentage of Ligilactobacillus and decreasing Alistipes and Barnesiella. In summary, we found that LP postbiotic was effective to protect broilers against Salmonella infection, possibly through suppressing NLRP3 inflammasome and optimizing gut microbiota. Our study provides the potential of postbiotics on prevention of Salmonella infection in poultry.
沙门氏菌感染是家禽生产中的一个主要问题，对食品安全构成潜在威胁。我们之前的研究证实，植物乳杆菌（LP）后生元在体外对沙门氏菌具有很强的抗菌能力。本研究旨在探讨 LP 后生元对沙门氏菌攻毒肉鸡的有益作用及其潜在机制。将 240 只 1 日龄雄性黄羽肉鸡用 0.8% deMan Rogosa Sharpe（MRS）培养基或 0.8% LP 后生元（LP 无细胞培养上清液，LPC）在饮用水中预处理 28d，然后用 1×10 CFU 肠炎沙门氏菌血清型肠炎亚种（SE）攻毒。感染后 3d 处死鸟类。结果表明，LPC 通过增加 SE 攻毒肉鸡的体重（BW）、平均日增重（ADG）和平均日采食量（ADFI）来维持生长性能。LPC 显著减轻 SE 诱导的肠道黏膜损伤。具体而言，它降低了肠道损伤评分，增加了绒毛长度和绒毛/隐窝，调节了与肠道损伤相关的基因（Villin、基质金属蛋白酶 3 [MMP3]、肠脂肪酸结合蛋白 [I-FABP]）的表达，并增强了紧密连接（闭合蛋白-1 [ZO-1]和 Claudin-1）。SE 感染引起了剧烈的炎症反应，表现为白细胞介素（IL）-1β、IL-6、TNF-α浓度上调，IL-10 下调，而 LPC 预处理明显逆转了这一趋势。我们发现 LPC 通过降低 Caspase-1、IL-lβ 和 IL-18 的基因表达来抑制 NOD 样受体热蛋白结构域相关蛋白 3（NLRP3）炎症小体的激活。此外，LPC 通过抑制核因子-κB（NF-κB）信号通路（降低 Toll 样受体 4 [TLR4]、髓样分化因子 88 [MyD88]和 NF-κB 的水平）来抑制 NLRP3 炎症小体的激活。最后，我们的结果表明，LPC 通过增强 Ligilactobacillus 的比例和降低 Alistipes 和 Barnesiella 来调节肠道微生物群。总之，我们发现 LP 后生元能有效保护肉鸡免受沙门氏菌感染，可能通过抑制 NLRP3 炎症小体和优化肠道微生物群。本研究为后生元在预防家禽沙门氏菌感染中的应用提供了可能。
