Chitosan and chitooligosaccharides attenuate soyabean meal-induced intestinal inflammation of turbot (Scophthalmus maximus): possible involvement of NF-кB, activator protein-1 and mitogen-activated protein kinases pathways

Abstract

AbstractAn 8-week feeding experiment was conducted to investigate and confront the putative functions of chitosan (CTS) and chitooligosaccharide (COS) in the growth and homoeostasis of distal intestine in juvenile turbots fed diets containing soyabean meal (SBM). Three isolipidic and isonitrogenous diets were formulated by supplemented basal diet (based on a 400 g/kg SBM) with 7·5 g/kg CTS or with 2·0 g/kg COS. Our results indicated that both CTS and COS supplementation could significantly improve (i) the growth performance and feed efficiency ratio; (ii) antioxidant activity driven by metabolic enzymes (i.e. catalase, glutathione reductase, glutathione peroxidase and superoxide dismutase); (iii) glutathione levels; (iv) acid phosphatase and lysozyme activity and (v) IgM content. As a result, these two particular prebiotics were able to significantly attenuate the histological alterations due to local inflammation as well as to decrease the transcriptional levels of proinflammatory cytokines (i.e. IL-1β, IL-8 and TNF-α) and major pathway effectors (i.e. activator protein-1 (AP-1), NF-кB, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase and extracellular regulated kinase). High-throughput sequencing data indicated that dietary CTS and COS could significantly decrease the diversity of intestinal bacteria but elevate the relative abundances of Bacillus, Lactobacillus and Pseudomonas genera. Altogether, these findings suggest that CTS and COS can improve growth of turbot, enhance intestinal immune and anti-oxidant systems and promote the balance of intestinal microbiota. The protective effects, elicited by these two prebiotics, against SBM-induced inflammation could be attributed to their roles in alleviating the overexpression of inflammatory cytokines by possibly down-regulating NF-кB, AP-1 and/or mitogen-activated protein kinases pathways.