Dietary chitosan oligosaccharides alleviate heat stress–induced intestinal oxidative stress and inflammatory response in yellow-feather broilers

The purpose of this study was to evaluate the effects of chitosan oligosaccharides (COS) on intestinal permeability, morphology, antioxidant status, and inflammatory response in heat-stressed broilers. A total of 108 thirty-five-day-old Chinese yellow-feather broilers (body weight 470.31 ± 13.15 g) were randomly allocated to 3 dietary treatments as follows: CON group, basal diet and raised under normal temperature (24°C); HS group, basal diet and raised under cycle heat stress (34°C from 10:00–18:00 and 24°C for the rest time); HSC group, basal diet with 200 mg/kg COS supplementation and raised under cycle heat stress. Each treatment had 6 replication pens and 6 broilers per pen. Compared with the CON group, heat stress decreased (P < 0.05) the relative weight of duodenum and jejunum; the relative length and villus height (VH) of duodenum, jejunum, and ileum; the ileum VH to crypt depth ratio; duodenum mucosal catalase (CAT) activity; and jejunum mucosal glutathione peroxidase (GSH-Px) and CAT activity, whereas it increased (P < 0.05) serum diamine oxidase (DAO) activity and D-lactate acid (D-LA) content, duodenum and jejunum mucosal malondialdehyde (MDA) and interleukin-1β (IL-1β) content, and ileum mucosal tumor necrosis factor-α content. Compared to the HS group, dietary COS supplementation increased (P < 0.05) the relative length of duodenum, jejunum, and ileum; the VH of jejunum and ileum; and duodenum and jejunum mucosal GSH-Px activity, whereas it decreased (P < 0.05) serum DAO activity and D-LA concentration and duodenum and jejunum mucosal MDA and IL-1β content. These results suggested that dietary COS supplementation had beneficial effects on intestinal morphology by increasing jejunum and ileum VH; permeability by decreasing serum DAO activity and D-LA content; antioxidant capacity by decreasing duodenum and jejunum mucosal MDA content and by increasing duodenum and jejunum GSH-Px activity; and inflammatory response by decreasing duodenum and jejunum mucosal IL-1β content.