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The objective of this study was to evaluate the modified hydrated sodium calcium aluminosilicate (HSCAS) adsorbent ability to reduce the toxicity of T-2 toxin in broilers. 96 one-day-old male broilers were randomly allocated to 4 experimental groups with 4 replicates of 6 birds each. The four groups 1–4 were received the basal diet (BD), BD plus 6.0 mg/kg T-2 toxin, BD plus 6.0 mg/kg T-2 toxin with 0.05% modified HSCAS adsorbent, BD plus 0.05% modified HSCAS adsorbent, respectively, for 2 weeks. The growth performance, nutrients digestibility, and digestive tract histopathology were analyzed. Compared with the control group, dietary supplementation of T-2 toxin decreased (P < 0.05) body weight gain, feed intake and feed conversion by 11.4–31.8% during d 1–7, d 8–14 and d 1–14. Dietary supplementation of T-2 toxin also decreased (P < 0.05) the apparent metabolic rate of crude protein, calcium, and total phosphorus by 14.9–16.1% during d 8–14. These alterations induced by T-2 toxin were mitigated or prevented (P < 0.05) by the supplementation of the modified HSCAS adsorbent. Meanwhile, dietary modified HSCAS adsorbent supplementation also prevented (P < 0.05) T-2 toxin-induced morphological changes and damage, such as severe degeneration and desquamation of the villous epithelial cells, congestion in intestinal lamina propria, and edema and thicken in the serosa with infiltration of numerous lymphoid cells, in the gizzard, duodenum, jejunum, and ileum of broilers. Notably, dietary supplementation of the modified HSCAS adsorbent alone did not affect (P > 0.05) any of those parameters. In conclusion, these findings indicate this novel HSCAS could be used as a promising adsorbent for protecting against T-2 toxin-induced toxicity in chicks (This work was supported in part by the National Key Research and Development Program of China, Projects 2018YFD0500601 and 2016YFD0501207).

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.

This study was conducted to determine the effect of T-2 toxin on the transcriptome of the glandular stomach in chicks using RNA-sequencing (RNA-Seq). Four groups of 1-day-old Cobb male broilers (n = 4 cages/group, 6 chicks/cage) were fed a corn-soybean-based diet (control) and control supplemented with T-2 toxin at 1.0, 3.0, and 6.0 mg/kg, respectively, for 2 weeks. The histological results showed that dietary supplementation of T-2 toxin at 3.0 and 6.0 mg/kg induced glandular gastric injury including serious inflammation, increased inflammatory cells, mucosal edema, and necrosis and desquamation of the epithelial cells in the glandular stomach of chicks. RNA-Seq analysis revealed that there were 671, 1393, and 1394 genes displayed ≥2 (P