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T-2 toxin-induced splenic injury by disrupting the gut microbiota-spleen axis via promoting IL-6/JAK/STAT1 signaling-mediated inflammation and apoptosis and its mitigation by elemental nano-selenium

文献类型： 外文期刊

作者： Liu, Meng 1 ; Li, Xue-Wu 1 ; Sun, Hua 3 ; Yan, Yi-Qin 1 ; Xia, Zhi-Yuan 1 ; Refaie, Alainaa 1 ; Zhang, Ni-Ya 1 ; Wang, Shuai 1 ; Tan, Chen 1 ; Sun, Lv-Hui 1 ;

作者机构： 1.Huazhong Agr Univ, Coll Anim Sci & Technol,Minist Agr & Rural Affairs, Frontiers Sci Ctr Anim Breeding & Sustainable Prod, State Key Lab Agr Microbiol,Key Lab Smart Farming, Wuhan 430070, Hubei, Peoples R China

2.Newhope Liuhe Co Ltd, Beijing, Peoples R China

3.Inner Mongolia Acad Agr & Anim Husb Sci, Hohhot 010031, Inner Mongolia, Peoples R China

关键词： T-2 toxin; Immunotoxicity; Gut microbiota-spleen axis; Nano-selenium; Mitigation

期刊名称：ARCHIVES OF TOXICOLOGY （ 影响因子：6.9； 五年影响因子：6.4 ）

ISSN： 0340-5761

年卷期： 2025 年 99 卷 6 期

页码：

收录情况： SCI

摘要： T-2 toxin is one of the most toxic A trichothecene mycotoxins prevalent in the environment and food chain, which brings severe health hazards to both animals and humans and it can significantly damage immune function. In this study, we comprehensively explained the impact of T-2 toxin on the spleen through gut microbiota-spleen axis by integrating the transcriptome and microbiome. Our results revealed that dietary T-2 toxin >= 1.0 mg/kg exposure significantly inhibited the growth performance and caused spleen injury in broilers chicks, accompanied by oxidative stress and histopathological damage. Cecal microbiome analysis suggested that T-2 toxin exposure caused gut microbial dysbiosis, especially leading to the decrease of some beneficial bacteria genera that enhanced gut barrier and reduced inflammation, including Blautia, Coprococcus, Lachnospira and Anaerostipes belonging to Lachnospiraceae family. Transcriptome analysis suggested that T-2 toxin exposure directly caused splenic inflammation and immune-related signaling, such as cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway, NOD-like receptor signaling pathway and JAK-STAT signaling pathway. Furthermore, by integrating the transcriptome and microbiome analysis, we found that spleen damage induced by T-2 toxin was associated with the abnormal activation of IL-6/JAK/STAT1 signaling pathway-mediated inflammation and apoptosis, which was further verified by western bolt analysis. Notably, dietary selenium supplementation could protect chicks from T-2 toxin-induced adverse effects on growth performance and spleen injury by inhibiting the expression of the IL-6/JAK/STAT1 signaling-related genes. In summary, our findings provided new insights into the immunotoxicity mechanisms of T-2 toxin in the chickens' spleen and highlighted the potential of selenium to alleviate T-2 toxin-induced immunotoxicity.

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