Abstract

Abstract This study was conducted to reveal the mechanism of T-2 toxin induced small intestine injuries in broilers through a new perspective that combined transcriptomics and microbiology studies. 96-d-old male Cobb broilers were randomly allocated into 4 treatment groups with 4 replicates of 6 birds/cage and all birds were fed a corn-soybean-based diet (Control) and the other 3 groups supplemented with T-2 toxin at 1.0, 3.0 or 6.0 mg/kg, respectively, for 2 weeks. Growth performance and nutrients digestibility were analyzed. Duodenum was collected to assay for histology, transcriptomics and microbiology. Compared with the control, final body weight, body weight gain and feed intake were decreased (P < 0.05) in a dose-dependent manner with increasing dietary T-2 toxin dose. Specially, in dietary T-2 toxin at 6.0 mg/kg, the feed/gain increased (P < 0.05) 11.4% and the apparent metabolic rate of crude protein, calcium and phosphorus were decreased (P < 0.05) by 14.9%, 18.0% and 16.1%, respectively. Meanwhile, T-2 toxin induced severe degeneration, necrosis and desquamation of the villous epithelial cells, increased inflammatory cells. Furthermore, the results of transcriptome drew that 2536 genes showed significant differences and were partially enriched in metabolic pathways, cell growth and death, apoptosis, the metabolism by CYP450, immune response pathways. Gut microbiota play a key role as microbial and duodenum genes and metabolites affected by T-2 toxin shared multiple pathways. Remarkably, Firmicutes and Proteobacteria that related to energy metabolism and inflammatory were seriously affected (P < 0.05). In summary, combined the results of integrated analysis, T-2 toxin partially induced intestine injury, potentially through changing the gene expression and the intestinal micro-ecology or damaging the intestinal mucosal directly, thus inducing inflammatory and apoptotic.

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