Yi Linyuan, Mo Aijie, Yang Huijun, Yang Yifan, Xu Qian, Yuan Yongchao
College of Fisheries, Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, Hubei, China.
Shuangshui Shuanglu Institute, Huazhong Agricultural University, Wuhan, China.
Front Immunol. 2025 Jan 15;15:1475195. doi: 10.3389/fimmu.2024.1475195. eCollection 2024.
Glycinin-induced foodborne enteritis is a significant obstacle that hinders the healthy development of the aquatic industry. Glycinin causes growth retardation and intestinal damage in hybrid yellow catfish ( ♀ × ♂), but its immune mechanisms are largely unknown. In the current study, five experimental diets containing 0% (CK), 1.74% (G2), 3.57% (G4), 5.45% (G6), and 7.27% (G8) immunological activity of glycinin were fed to juvenile hybrid yellow catfish to reveal the mechanism of the intestinal immune response to glycinin through RNA and microRNA (miRNA) sequencing and to explore the interrelation between immune molecules and intestinal microbiota. The results demonstrated that glycinin content in the posterior intestine increased significantly and linearly with the rise of dietary glycinin levels. More than 5.45% of dietary glycinin significantly reduced the nutritional digestion and absorption function of the posterior intestine. Notably, an obvious alteration in the expression levels of inflammatory genes (, , , and ) of the posterior intestine was observed when dietary glycinin exceeded 3.57%. Sequencing results of RNA and miRNA deciphered 4,246 differentially expressed genes (DEGs) and 28 differentially expressed miRNAs (DEmiRNAs) between the CK and G6 groups. Furthermore, enrichment analysis of DEGs and DEmiRNA target genes exhibited significant responses of the MAPK, NF-κB, and WNT pathways following experimental fish exposure to 5.45% dietary glycinin. Additionally, at the level of 3.57% in the diet, glycinin obviously inhibited the increase of microbiota, especially potential probiotics such as , , , and . In sum, 5.45% dietary glycinin through the MAPK/NF-κB/WNT pathway induces enteritis, and inflammatory conditions could disrupt micro-ecological equilibrium through miRNA secreted by the host in hybrid yellow catfish. This study constitutes a comprehensive transcriptional perspective of how intestinal immunity responds to excessive glycinin in fish intestines.
大豆球蛋白诱导的食源性肠炎是阻碍水产业健康发展的一个重大障碍。大豆球蛋白会导致杂交黄颡鱼（♀×♂）生长迟缓并造成肠道损伤，但其免疫机制在很大程度上尚不清楚。在本研究中，将含有0%（对照）、1.74%（G2）、3.57%（G4）、5.45%（G6）和7.27%（G8）免疫活性大豆球蛋白的五种实验饲料投喂给杂交黄颡鱼幼鱼，通过RNA和微小RNA（miRNA）测序揭示肠道对大豆球蛋白免疫反应的机制，并探索免疫分子与肠道微生物群之间的相互关系。结果表明，后肠中大豆球蛋白的含量随着饲料中大豆球蛋白水平的升高而显著且呈线性增加。饲料中大豆球蛋白含量超过5.45%会显著降低后肠的营养消化和吸收功能。值得注意的是，当饲料中大豆球蛋白超过3.57%时，观察到后肠炎症基因（、、、和）的表达水平发生明显变化。RNA和miRNA的测序结果解析了对照和G6组之间4246个差异表达基因（DEG）和28个差异表达miRNA（DEmiRNA）。此外，对DEG和DEmiRNA靶基因的富集分析显示，实验鱼暴露于5.45%的饲料大豆球蛋白后，丝裂原活化蛋白激酶（MAPK）、核因子κB（NF-κB）和WNT信号通路出现显著反应。此外，在饲料中大豆球蛋白含量为为3.57%时，大豆球蛋白明显抑制微生物群的增加，尤其是潜在的益生菌，如、、、和。总之，饲料中5.45%的大豆球蛋白通过MAPK/NF-κB/WNT信号通路诱发肠炎，并通过宿主分泌的miRNA破坏杂交黄颡鱼的微生态平衡。本研究从转录角度全面阐述了鱼类肠道免疫对过量大豆球蛋白的反应。
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