Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 225, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2021.112786
Keywords
Zearalenone; Immune; Pathogen infection; Mucus layer; Grass carp
Categories
Funding
- National Natural Science Foundation of China [31922086]
- National Key Research and Development Program of China [2018YFD0900400, 2019YFD0900200]
- Earmarked Found for China Agriculture Research System [CARS-45]
- Sichuan Science and Technology Program [2019YFN0036]
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The study discussed the effects of zearalenone on intestinal immune components, cytokines and molecular mechanisms of juvenile grass carp, pointing out that zearalenone inhibits immune components in the intestines and may increase the risk of mucosal exposure and associated diseases.
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 mu g 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 beta-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 kappa B (NF-kappa B) 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.
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