Low intestinal inflammation model (HP48) in Atlantic salmon (Salmo salar) and inflammatory mitigation by Bactocell

• Published in: Aquaculture
• Main Authors: Nordvi, Malene Fosse, Løvmo, Signe Dille, Whatmore, Paul, Sundh, Henrik, Sigholt, Trygve, Olsen, Rolf Erik
• Format: Article in Journal/Newspaper
• Language: English
• Published: Elsevier Science 2022
• Subjects: Atlantic salmon; Salmo salar
• Online Access: https://hdl.handle.net/11250/3029494; https://doi.org/10.1016/j.aquaculture.2022.738920

Moderate levels of intestinal damage and inflammation are often seen in intensive fish aquaculture. The causes may be due to antinutrients from plant meals, stress or other causes. There is currently a lack of good models to explore these effects and so how to mitigate the consequences. Most studies have used full-fat soy or other compounds that cause intestinal damage that are likely not reversible. In this study we have explored the possibility of using soybean HP48, made from solvent extracted peeled soybeans, as a low-inflammation model in post-smolt Atlantic salmon, and then investigated whether supplementation of the probiotic Pediococcus acidilactici CNCM I-4622 – MA 18/5 M (Bactocell) could diminish this effect. The fish were fed triplicate diets. A Control diet containing 18.08% soy protein concentrate (SPC), a HP48 diet where most of the SPC was replaced by HP48 (5.00% SPC and 17.68% HP48), and a Bactocell diet that was identical to the HP48 diet but contained 0.03% Bactocell. After 10 weeks of feeding, the mid- and hind-intestinal health were assessed by histology, integrity (Ussing chamber) and gene expression (RNAseq). Transcriptomic and integrity data suggests that HP48 led to a disturbed mid-intestinal homeostasis with impaired cellular integrity and increased inflammation and cell turnover. Most of the transcriptomic effects were reversed with Bactocell including downregulation of immune genes and upregulation of transmembrane proteins such as type IV collagen, which is important in restoring epithelial homeostasis. In the hind-intestine, the HP48 diet led to deleterious morphological changes such as widening of lamina propria and stratum granulosum, disrupted mucosal folds, loss of absorptive vacuoles, and upregulation of several immune regulated genes and downregulation of genes involved in solute- and water transport. The intestinal integrity assessed by Ussing chamber was not affected. Bactocell supplementation did alleviate several of the morphological effects. However, it was not able to ...