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T-2 toxin-induced intestinal damage with dysregulation of metabolism, redox homeostasis, inflammation, and apoptosis in chicks

  • Organ Toxicity and Mechanisms
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Abstract

T-2 toxin is a worldwide problem for feed and food safety, leading to livestock and human health risks. The objective of this study was to explore the mechanism of T-2 toxin-induced small intestine injury in broilers by integrating the advanced microbiomic, metabolomic and transcriptomic technologies. Four groups of 1-day-old male broilers (n = 4 cages/group, 6 birds/cage) were fed a control diet and control diet supplemented with T-2 toxin at 1.0, 3.0, and 6.0 mg/kg, respectively, for 2 weeks. Compared with the control, dietary T-2 toxin reduced feed intake, body weight gain, feed conversion ratio, and the apparent metabolic rates and induced histopathological lesions in the small intestine to varying degrees by different doses. Furthermore, the T-2 toxin decreased the activities of glutathione peroxidase, thioredoxin reductase and total antioxidant capacity but increased the concentrations of protein carbonyl and malondialdehyde in the duodenum in a dose-dependent manner. Moreover, the integrated microbiomic, metabolomic and transcriptomic analysis results revealed that the microbes, metabolites, and transcripts were primarily involved in the regulation of nucleotide and glycerophospholipid metabolism, redox homeostasis, inflammation, and apoptosis were related to the T-2 toxin-induced intestinal damage. In summary, the present study systematically elucidated the intestinal toxic mechanisms of T-2 toxin, which provides novel ideas to develop a detoxification strategy for T-2 toxin in animals.

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Acknowledgements

This research was funded by the Open Project of the Key Laboratory of Animal Embryo Engineering and Molecular Breeding of Hubei Province (KLAMEMB-2017-05); the National Key Research and Development Program of China, Project (2016YFD0501207 and 2018YFD0500601); and a gift from Jiangsu Aomai Bio-technology Co., Ltd.

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  1. Meng Liu and Ling Zhao have contributed equally to this paper.

Authors and Affiliations

  1. State Key Laboratory of Agricultural Microbiology, Key Laboratory of Animal Embryo Engineering and Molecular Breeding of Hubei Province, Hubei Hongshan Laboratory, Frontiers Science Center for Animal Breeding and Sustainable Production, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan, 430070, Hubei, China

    Meng Liu, Ling Zhao, Jin-Tao Wei, Yu-Xuan Huang & Lv-Hui Sun

  2. Institute of Animal Husbandry and Veterinary Sciences, Hubei Academy of Agricultural Sciences, Wuhan, 430064, China

    Jin-Tao Wei

  3. Monogastric Research Center, School of Agriculture and Environment, Massey University, Palmerston North, 4442, New Zealand

    Mahmoud Mohamed Khalil

  4. MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China

    Wen-Da Wu

  5. Department of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanskeho 62, 50003, Hradec Kralove, Czech Republic

    Kamil Kuča

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Contributions

LHS and JTW designed the research; ML, LZ, JTW, and YXH conducted the experiments and analyzed the data; LM, ZL, and LHS wrote the paper; MMK, WDW, KK help review and edit the paper; LHS had the primary responsibility for the final content. All authors read and approved the final manuscript.

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Correspondence to Jin-Tao Wei or Lv-Hui Sun.

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Liu, M., Zhao, L., Wei, JT. et al. T-2 toxin-induced intestinal damage with dysregulation of metabolism, redox homeostasis, inflammation, and apoptosis in chicks. Arch Toxicol 97, 805–817 (2023). https://doi.org/10.1007/s00204-023-03445-z

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