LPS-Induced Liver Injury of Magang Geese through Toll-like Receptor and MAPK Signaling Pathway

Simple Summary LPS is one of the main virulence factors of Gram-negative bacteria. In the breeding process of geese, due to the influence of environmental factors, harmful bacteria easily breed in the water body, resulting in an increase in the concentration of LPS in the goose. The liver has an important function of clearing LPS, but excess LPS can induce liver damage, resulting in a reduced production performance for the goose. In our study, we found that LPS induces inflammatory damage in the liver. Further, through transcriptome sequencing analysis, we screened 727 differentially expressed genes for LPS-induced liver injury, and we performed enrichment analysis. The results showed that LPS-induced liver injury in geese may be the result of the joint action of Toll-like receptor, MAPK, NOD-like receptor, FoxO, and PPAR signaling pathway. Among them, the TLR7-mediated MAPK signaling pathway plays a major role. Lipopolysaccharide (LPS) is one of the main virulence factors of Gram-negative bacteria. In the process of waterfowl breeding, an inflammatory reaction due to LPS infection is easily produced, which leads to a decline in waterfowl performance. The liver plays a vital role in the immune response and the removal of toxic components. Therefore, it is necessary to study the mechanism of liver injury induced by LPS in goose. In this study, a total of 100 1-day-old goslings were randomly divided into a control group and LPS group after 3 days of pre-feeding. On days 21, 23, and 25 of the formal experiment, the control group was intraperitoneally injected with 0.5 mL normal saline, and the LPS group was intraperitoneally injected with LPS 2 mg/(kg body weight) once a day. On day 25 of the experiment, liver samples were collected 3 h after the injection of saline and LPS. The results of histopathology and biochemical indexes showed that the livers of the LPS group had liver morphological structure destruction and inflammatory cell infiltration, and the levels of ALT and AST were increased. Next, RNA sequencing analysis was used to determine the abundances and characteristics of the transcripts, as well as the associated somatic mutations and alternative splicing. We screened 727 differentially expressed genes (DEGs) with p < 0.05 and |log(2)(Fold Change)| >= 1, as the thresholds; GO and KEGG enrichment analysis showed that LPS-induced liver injury may be involved in the Toll-like receptor signaling pathway, MAPK signaling pathway, NOD-like receptor signaling pathway, FoxO, and PPAR signaling pathway. Finally, we intersected the genes enriched in the key pathway of LPS-induced liver injury with the top 50 key genes in protein-protein interaction networks to obtain 28 more critical genes. Among them, 17 genes were enriched in Toll-like signaling pathway and MAPK signaling pathway. Therefore, these results suggest that LPS-induced liver injury in geese may be the result of the joint action of Toll-like receptor, MAPK, NOD-like receptor, FoxO, and PPAR signaling pathway. Among them, the TLR7-mediated MAPK signaling pathway plays a major role.

Automated summary

LPS is a virulence factor of Gram-negative bacteria and its excessive concentration in geese can induce liver damage and reduce production performance. In this study, transcriptome sequencing analysis identified 727 differentially expressed genes related to LPS-induced liver injury and enrichment analysis showed the involvement of Toll-like receptor, MAPK, NOD-like receptor, FoxO, and PPAR signaling pathways. The TLR7-mediated MAPK signaling pathway played a major role in LPS-induced liver injury in geese.