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The Evaluation of MAPK/ERK Signaling Pathway in Chicken Necrotic Enteritis Based on Microbiomics and Metabolomics
Chicken necrotic enteritis is a prevalent intestinal disease caused by Clostridium perfringens (C. perfringens) in chickens. Previous research has confirmed the close relationship between the gut microbiota and its metabolites in connection with chicken necrotic enteritis. However, it remains unclear how the gut microbiota of the host influences host metabolism following the onset of necrotic enteritis (NE). The close relationship between gut microbiota and their metabolites in chicken necrotic enteritis (NE) has been established, yet the metabolic influence of microbiota post-NE onset remains unclear. In this study, 1-day-old White Leghorn chickens were divided into three groups (n=10/group), a negative control (CON) fed a basal diet, a fishmeal-supplemented group (F) receiving 50% fishmeal, and an NE group inoculated orally with C. perfringens alongside fishmeal supplementation. Growth performance, intestinal lesions, and morphological changes were recorded. Cecal contents were subjected to 16S rDNA sequencing for microbiota profiling, while serum metabolomics was analyzed via LC-MS.No noticeable damage was observed in the small intestines of the F group, whereas the NE group exhibited marked body weight reduction. Cell necrosis and jejunal mucosal shedding were identified, accompanied by ileal villi atrophy and significant reductions in tight junction proteins (Claudin-1 and ZO-1). Both F and NE groups showed decreased cecal abundances of Lactobacillus and Blautia, alongside increased Clostridium and Escherichia coli. Serum metabolomics revealed distinct glycerophospholipid and arginine-proline metabolism alterations in the F group versus CON. In contrast, NE-associated metabolic shifts were linked to pathways regulating cell proliferation, differentiation, and migration, particularly MAPK signaling. Downregulation of MAPK/ERK pathway genes was detected in the jejunal mucosa of infected chickens compared to CON and F groups. Concurrently, jejunal PCNA expression was quantified and found to be significantly reduced in the NE cohort relative to controls. Drawing upon the experimental results, it was concluded that necrotic enteritis in chickens was linked to a disruption in the intestinal epithelial barrier. Additionally, alterations in the gut microbiota hindered the activation of the MAPK/ERK signaling pathway, which in turn reduced the proliferation of intestinal epithelial cells and impaired the repair processes crucial for intestinal barrier restoration.
The Evaluation of MAPK/ERK Signaling Pathway in Chicken Necrotic Enteritis Based on Microbiomics and Metabolomics (Text)
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