Dietary Probiotic Bacillus licheniformis H2 Enhanced Growth Performance, Morphology of Small Intestine and Liver, and Antioxidant Capacity of Broiler Chickens Against Clostridium perfringens-Induced Subclinical Necrotic Enteritis.

The reduction in the use of antibiotics in the poultry industry has considerably increased the appearance of Clostridium perfringens (CP)-induced subclinical necrotic enteritis (SNE), forcing researchers to search alternatives to antibiotic growth promoters (AGP) like probiotics. This study aimed to investigate the effect and the underlying potential mechanism of dietary supplementation of Bacillus licheniformis H2 to prevent SNE. A total of 180 1-day-old male broiler chickens (Ross 308) were randomly divided into three groups, with six replicates in each group and ten broilers per pen: (a) basal diet in negative control group(NC group); (b) basal diet + SNE infection(coccidiosis vaccine + CP) (SNE group); (c) basal diet + SNE infection + H2 pre-treatment(BL group). Growth performance, morphology of small intestine and liver, and antioxidant capacity of the serum, ileum, and liver were assessed in all three groups. The results showed that H2 significantly suppressed (P < 0.05) the negative effects on growth performance induced by SNE, including loss of body weight gain, decrease of feed intake, and raise of feed conversion ratio among the different treatments at 28 days. The addition of H2 also increased (P < 0.05) the villus height: crypt depth ratio as well as villus height in the ileum. Chicks fed with H2 diet had lower malondialdehyde (MDA) concentration in the ileum in BL group than that in SNE group (P < 0.05). Moreover, compared with other treatment groups, dietary H2 improved the activities of antioxidant enzymes in the ileum, serum, and liver (P < 0.05). H2 may also prevent SNE by significantly increasing the protein content (P < 0.05) of Bcl-2 in the liver. Dietary supplementation of H2 could effectively prevent the appearance of CP-induced SNE and improve the growth performance of broiler chickens damaged by SNE, of which the mechanism may be related to intestinal development, antioxidant capacity, and apoptosis which were improved by H2.