The occurrence of immuno-compromised status in animals with zearalenone (ZEA) exposure may be a critical contributor to associated mucosal (gastrointestinal tract) diseases. However, it is difficult to assess the associated risks with limited reference data. This study comprehensively discussed the effects of ZEA on intestinal immune components, cytokines and molecular mechanism of juvenile grass carp infected with Aeromonas hydrophila. Specifically, the fish were fed six graded levels of dietary ZEA (0–2507 μg kg⁻¹ diet) for 70 d. The results pointed out that the average residual amount of ZEA in the intestines increased with dose level after ZEA feeding. We further performed an infection assay using A. hydrophila. After 14 d, ZEA groups increased enteritis morbidity rate compared with controls. The acid phosphatase (ACP), lysozyme (LZ) activities and immunoglobulin M (IgM) content were significantly decreased in three intestinal segments. Furthermore, ZEA could reduce the transcription of β-defensin-1, Hepcidin, liver expressed antimicrobial peptide 2A/2B (LEAP-2A/2B) and Mucin-2. We next confirmed the loss of these immune components accompanied by the invasion of the intestinal barrier by bacteria, as indicated by activation of the nuclear factor κB (NF-κB) and the expression of downstream cytokines. Notably, the phosphorylated target of rapamycin (TOR) plays an important role in regulating these genes, thus indicating a possible target caused by ZEA. In summary, the extensive inhibition of immune components by ZEA promotes the spread of pathogens, which may increase the possibility of intestinal mucosa exposure and the risk of transforming disease.

暴露于玉米赤霉烯酮 (ZEA) 的动物出现免疫受损状态可能是导致相关粘膜（胃肠道）疾病的关键因素。然而，用有限的参考数据很难评估相关风险。本研究综合探讨了玉米淀粉对嗜水气单胞菌感染幼草鱼肠道免疫成分、细胞因子及分子机制的影响。具体而言，将鱼喂食六种等级的日粮 ZEA（0-2507 μg kg ^-1日粮）70 天。结果表明，ZEA饲喂后，ZEA在肠道中的平均残留量随着剂量水平的增加而增加。我们进一步使用A. hydrophila进行了感染测定. 14 d 后，与对照组相比，ZEA 组增加了肠炎发病率。三个肠段的酸性磷酸酶 (ACP)、溶菌酶 (LZ) 活性和免疫球蛋白 M (IgM) 含量显着降低。此外，ZEA 可以减少β-defensin-1、Hepcidin、肝脏表达的抗菌肽 2A/2B ( LEAP-2A/2B ) 和Mucin-2的转录. 我们接下来证实了这些免疫成分的丧失伴随着细菌侵入肠道屏障，如核因子 κB (NF-κB) 的激活和下游细胞因子的表达所表明的。值得注意的是，雷帕霉素的磷酸化靶标（TOR）在调节这些基因中起重要作用，因此表明可能是由 ZEA 引起的靶标。综上所述，ZEA对免疫成分的广泛抑制促进了病原体的传播，这可能会增加肠黏膜暴露的可能性和转化疾病的风险。