Effects of Lactobacillus acidophilus on the growth performance, immune response, and intestinal barrier function of broiler chickens challenged with Escherichia coli O157

Abstract

We studied the effects of Lactobacillus acidophilus (L. acidophilus) on the growth performance, intestinal morphology, barrier function, and immune response of broilers challenged with Escherichia coli O157 (E. Coli). A total of 360 1-day-old Cobb male broilers were tested in a 3 × 2 factorial arrangement with 3 dietary L. acidophilus levels (0, 5 × 108 CFU/kg, and 10 × 108 CFU/kg of diet) and 2 disease challenge treatments (control or E. coli challenged). Results showed that E. coli challenge decreased the ADG, ADFI, and BW of broilers from 15 to 21 d (P < 0.05), increased the jejunum intestinal wall thickness, and significantly increased the mortality rate. E. coli challenge significantly (P < 0.05) decreased the serum IgA and IgM contents and peripheral blood CD3+ T cell counts (P < 0.05), increased the serum CRP, DAO, and LPS levels at 21 d; upregulated the mRNA expression of iNOS, IL-8, IL-1β in the jejunum and iNOS in the spleen, and downregulated the occludin and ZO-1 mRNA expression in the ileum at 21 d compared with uninfected birds (P < 0.05). Dietary L. acidophilus supplementation consistently showed higher BW, ADG, ADFI, and jejunum and ileum V:C ratio at 14 d and 21 d in the presence and absence of E. coli challenge (P < 0.05). L. acidophilus supplementation reduced the mortality rate caused by E. coli challenge (P < 0.05), decreased the serum CRP, DAO, and LPS levels at 14 d and 21 d; upregulated the mRNA expression of occludin and ZO-1 in the jejunum and ileum, and downregulated the mRNA expression of iNOS, IL-8, and IL-1β in the jejunum in E. coli challenged birds at 21 d (P < 0.05). Dietary supplementation with L. acidophilus can improve the growth performance, intestinal health, and survival of broilers challenged with E. coli.

Keywords: Escherichia coli; Lactobacillus acidophilus; broiler; intestinal barrier function.