School of Animal Science and Veterinary Medicine, Jiangsu Vocational College of Agriculture and Forestry, Jurong, China212400 and College of Animal Science and Technology, Chinese Agricultural University, Beijing, China100093.
School of Animal Science and Veterinary Medicine, Jiangsu Vocational College of Agriculture and Forestry, Jurong, China212400 and College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China210095.
Food Funct. 2021 Jul 5;12(13):5913-5926. doi: 10.1039/d1fo01158h.
The aim of this study was to investigate the effects and potential signaling pathway of selenium-enriched Bacillus subtilis (SEBS) on beta defensin 1 (BD1) expression in chicken intestine. Chinese Huainan Partridge chickens (500 individuals) were randomly allocated into five groups, including control, inorganic Se, B. subtilis, SEBS, and a mixture of Se and B. subtilis (Se-BS). After 56 d of feeding, chicken ileal mucous membranes were harvested to detect differences in expression of BD1. The results indicated that BD1 was produced in intestinal crypt cells and secreted into the lumen through the villi brush border. BD1 was up-regulated in distal ileum segments colonized by SEBS and B. subtilis. Chicken primary intestinal crypt cells were cultured and grouped into control, inorganic Se, B. subtilis, SEBS, and Se-BS treatments to identify the receptor of B. subtilis. Results indicated that B. subtilis and SEBS were recognized by toll-like receptor 2 (TLR2), stimulating the NF-κB1 signaling pathway to increase expression of BD-1, which was further enhanced when combined with Se. Pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were up-regulated with B. subtilis supplementation, and inhibited under the action of Se. In conclusion, B. subtilis and SEBS were recognized by the TLR2 receptor in the ileal mucous membrane, which activated the TLR2-MyD88-NF-κB1 signaling pathway to upregulate BD1 expression. In addition, Se enhanced recognition of B. subtilis and reduced levels of pro-inflammatory factors caused by estrogenic B. subtilis supplementation.
本研究旨在探讨富硒枯草芽孢杆菌（SEBS）对鸡肠道β防御素 1（BD1）表达的影响及其潜在信号通路。将 500 只中国淮南麻鸭随机分为 5 组，分别为对照组、无机硒组、枯草芽孢杆菌组、SEBS 组和硒-枯草芽孢杆菌混合物组（Se-BS 组）。饲养 56d 后，采集鸡回肠黏膜，检测 BD1 表达差异。结果表明，BD1 由肠隐窝细胞产生，并通过绒毛刷状缘分泌到腔中。SEBS 和枯草芽孢杆菌定植的回肠远端段 BD1 表达上调。体外培养鸡原代肠隐窝细胞，分为对照组、无机硒组、枯草芽孢杆菌组、SEBS 组和 Se-BS 组，鉴定枯草芽孢杆菌的受体。结果表明，枯草芽孢杆菌和 SEBS 被 TLR2 识别，激活 NF-κB1 信号通路，增加 BD-1 的表达，与硒联合使用时表达进一步增强。促炎细胞因子 TNF-α、IL-1β 和 IL-6 随着枯草芽孢杆菌的补充而上调，并在硒的作用下受到抑制。综上所述，SEBS 被回肠黏膜 TLR2 受体识别，激活 TLR2-MyD88-NF-κB1 信号通路，上调 BD1 表达。此外，硒增强了对枯草芽孢杆菌的识别，并降低了枯草芽孢杆菌补充引起的促炎因子水平。
