Transcriptome analysis revealed ameliorative effect of probiotic Lactobacillus johnsonii BS15 against subclinical necrotic enteritis induced hepatic inflammation in broilers.

ABSTRACT

Subclinical necrotic enteritis (SNE) broadly occurs in boilers, which reduces the growth performance by causing serious economic and social problems. The following study was conducted to better understand the molecular mechanism of the SNE on liver inflammation and to examine the innovative prevention of Lactobacillus johnsonii BS15 upon SNE. The research was based on the regulatory molecular mechanism of Lactobacillus johnsonii BS15, and its effect on liver inflammatory pathways in the broiler with SNE infection. Day old one hundred and eighty (Cobb 500) broiler chickens were distributed into 3 groups (control, SNE and BS15 group) and reared for 28 days. RNA sequencing was used for the analysis of gene expression extracted from liver samples. Gene expression was detected with the help of quantitative real-time PCR (qRT-PCR). RNA-Seq analysis revealed altered expressions of genes involved in liver inflammatory pathway. A total number of 385 genes were found as differentially expressed (DEGs) in the liver samples that belonged to SNE group as compared with the control liver samples (p < 0.05). Out of those 385 genes, 117 were down-regulated and 268 were up-regulated. The DEGs related to liver inflammation between control group and SNE group or SNE and BS15 groups, included cluster of differentiation 80 (CD80), Interleukin 1 beta (IL1B), Phosphoinositide 3- Kinase regulatory subunit 5 (PIK3R5), Toll-like receptor 4 (TLR4), Toll-like receptor 2 A (TLR2A), and proto-oncogene protein (FOS). The RNA-Seq analysis provided DEGs expression and this result was validated by qRT-PCR. Results confirmed that these genes are essential in the regulation of liver inflammation in the SNE infected chickens. Findings of current research indicated that the hepatic inflammation could be induced by SNE in broilers. Simultaneously, effects of SNE infection on liver could be subsided by improved TLRs signaling pathway with the naturally present prophylactic strategy as BS15.