Abstract
This experiment investigated the effects of dietary tryptophan (Trp) supplementation on growth performance and intestinal health in broiler chickens challenged with Clostridium perfringens, and explored the underlying molecular mechanism. A total of 384 one-day-old Arbor Acres broiler chickens were randomly allocated in a 3 × 2 factorial design with three dietary Trp levels (0%, 0.1%, and 0.2%) and two infection statuses (with or without C. perfringens challenge). The results showed that 0.1% Trp supplementation significantly increased C. perfringens-induced decrease in ADG and ADFI during days 14-21 (P < 0.05). Additionally, 0.1% and 0.2% Trp supplementation significantly decreased the feed-to-gain ratio during days 14-21 (P < 0.05). Only 0.1% Trp supplementation significantly alleviated the decrease in serum IgA and IgG levels induced by C. perfringens (P < 0.05). C. perfringens challenge significantly increased IL-6 level (P < 0.05) and decreased IL-10 level in the serum (P < 0.05). Only 0.1% Trp supplementation significantly reduced IL-1β and IL-6 levels (P < 0.05) and elevated IL-10 level (P < 0.05). Dietary 0.1% Trp supplementation significantly attenuated the jejunal morphological injury induced by C. perfringens challenge (P < 0.05). Only 0.1% Trp supplementation significantly alleviated C. perfringens challenge-induced upregulation of jejunal IL-1β mRNA expression and downregulation of jejunal IL-10, IL-22, occludin and ZO-1 mRNA expression (P < 0.05). C. perfringens challenge significantly decreased serum serotonin level, and downregulated jejunal AhR and IDO2 mRNA expression (P < 0.05). Dietary 0.1% Trp supplementation significantly increased serum serotonin level and upregulated jejunal TPH1, IDO2, AhR and CYP1A1 mRNA expression (P < 0.05). In conclusion, dietary 0.1% Trp supplementation significantly enhanced immune function, mitigated intestinal injury, and improved growth performance in broiler chickens challenged with C. perfringens. These beneficial effects may be mediated through the activation of the AhR/CYP1A1 signaling pathway. However, the effects of 0.2% Trp supplementation were not as favorable as those of 0.1%.