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Abstract
Restrictions on the use of antibiotic growth promoters led to the reemergence of necrotic enteritis (NE), necessitating the development of alternatives. Two experiments were conducted to determine the ideal level of arginine essential to restore the NE-induced loss in growth performance, gut microbial homeostasis, and cecal short-chain fatty acid (SCFA) profile and elicit sufficient immune response in broilers during NE. In the first experiment, the 125% and 135% arginine diets were used to assess the efficiency of arginine in reversing the effect of sub-clinical NE on the growth, immune response, and gut microbial homeostasis of broilers. The 125% arginine diet reversed the NE-induced loss in body weight gain by 70g (p = 0.12) and increased the bile anti-C. perfringens IgA concentration (p < 0.01), the ratio of CD8+:CD4+ cells in the spleen on days 28 (p=0.01) and day 35 (p < 0.01) and the relative gene expression of IFN-γ (p < 0.01). The 125% arginine diet also restored the abundance of Bacteroidota (p = 0.03), Marinifilaceae (p = 0.03), Odoribacter (p = 0.03), O. splanchnicus (p = 0.03), and Mediterraneibacter cottocaccae (p < 0.01). The 135% arginine diet did not have a significant effect on the growth performance and immune response during NE but efficiently restored the gut microbial homeostasis. Considering the overall effect, a second experiment was conducted to evaluate the effect of a 125% arginine diet on growth, immune response, and microbial homeostasis in a clinical NE model. A significant challenge × diet interaction effect was observed in the cecal tonsil and spleen CD8+: CD4+ T-cell ratio on days 21 (p < 0.01 and p = 0.03) and 28 (p = 0.02 and p = 0.03), respectively. A significant interaction effect was also observed on the relative expression of the iNOS gene (p = 0.01) on day 21. However, the 125% arginine diet could not effectively restore the gut microbial homeostasis and SCFA profile during clinical NE. In conclusion, a 125% arginine diet had beneficial effects on growth performance, immune response, and gut microbial homeostasis during subclinical NE, but did not alleviate the disease pathologies during clinical NE.