Dietary Deoxynivalenol (DON) May Impair the Epithelial Barrier and Modulate the Cytokine Signaling in the Intestine of Atlantic Salmon ( Salmo salar )

• Published in: Toxins 2018-09, Vol.10 (9), p.376
• Main Authors: Moldal, Torfinn, Bernhoft, Aksel, Rosenlund, Grethe, Kaldhusdal, Magne, Koppang, Erling Olaf
• Format: Article
• Language: English
• Subjects: Antigens; Aquaculture; Aquaculture feeds; atlantic salmon; Carp; Cereals; Contamination; Cytokines; Deoxynivalenol; feed; Feeds; Fish; Fish oils; Gene expression; Immunity; Inflammation; Inflammatory response; Intestine; Markers; Mycotoxins; PCR; Proliferating cell nuclear antigen; Proteins; Salmo salar; Salmon; Signaling; suppressor of cytokine signaling; Suppressors; tight junctions; Trout; Weight
• ISSN: 2072-6651; 2072-6651
• DOI: 10.3390/toxins10090376

Impaired growth, immunity, and intestinal barrier in mammals, poultry, and carp have been attributed to the mycotoxin deoxynivalenol (DON). The increased use of plant ingredients in aquaculture feed implies a risk for contamination with mycotoxins. The effects of dietary DON were explored in 12-month-old Atlantic salmon ( ) (start weight of 58 g) that were offered a standard feed with non-detectable levels of mycotoxins (control group) or 5.5 mg DON/kg feed (DON group). Each group comprised two tanks with 25 fish per tank. Five fish from each tank were sampled eight weeks after the start of the feeding trial, when mean weights for the control and DON groups were 123.2 g and 80.2 g, respectively. The relative expression of markers for three tight junction proteins (claudin 25b, occludin, and tricellulin) were lower, whereas the relative expression of a marker for proliferating cell nuclear antigen was higher in both the mid-intestine and the distal intestine in fish fed DON compared with fish from the control group. The relative expression of markers for two suppressors of cytokine signaling (SOCS1 and SOCS2) were higher in the distal intestine in fish fed DON. There was no indication of inflammation attributed to the feed in any intestinal segments. Our findings suggest that dietary DON impaired the intestinal integrity, while an inflammatory response appeared to be mitigated by suppressors of cytokine signaling. A dysfunctional intestinal barrier may have contributed to the impaired production performance observed in the DON group.