Intestinal differential metabolite tryptophan from avian pathogenic Escherichia coli (APEC)-resistant and susceptible chickens alleviates APEC symptoms in chickens.

Abstract

To identify an effective antibiotic to combat avian pathogenic Escherichia coli (APEC), differential metabolites in the intestines of APEC-resistant and susceptible chickens were investigates. The effect of supplementing the diet of APEC-challenged chickens with the differential metabolite tryptophan was investigated. Tryptophan was identified as an important differential gut metabolite (APEC-resistant and susceptible chickens) using tryptophan-targeted metabolism detection. A total of 120 one-day-old chickens were divided into four groups: with and without 0.1 % tryptophan supplementation in the basal diet with and without APEC challenge. The APEC challenge test was conducted after an adaptation period of 8 days. The infection lasted 7 days, during which dead chickens were subjected to pathological autopsy, and the mortality rate was recorded. All chickens were slaughtered at the end of the infection test to calculate morbidity. Dietary supplementation with tryptophan did not significantly affect mortality in APEC-challenged chickens (P > 0.05) but significantly reduced their morbidity (P < 0.05). Dietary tryptophan supplementation reversed the elevated splenic gene expression of IL-6, TLR4, and NF-&#x3ba;B induced by the APEC challenge in chickens (P < 0.05). Tryptophan supplementation also alleviated the APEC-induced upregulation of the pro-inflammatory factors IL-6, IFN-&#x3b3;, and IL-1&#x3b2; in the blood (P < 0.05). Simultaneously, dietary supplementation with tryptophan significantly increased glutathione peroxidase activity and total antioxidant capacity level in the blood of APEC-challenged chickens (P < 0.05). Thus, APEC challenging in chickens induced organ damage, up-regulated inflammation-related gene expression in the spleen, and increased the levels of inflammatory factors in the blood. Dietary supplementation with tryptophan inhibited the production of inflammatory factors, possibly through the TLR4/NF-&#x3ba;B signaling pathway and attenuated the morbidity and the inflammatory response caused by the APEC challenge.