Fuente: PubMed "nature biotechnology" Poult Sci. 2026 Aug 3;105(11):107550. doi: 10.1016/j.psj.2026.107550. Online ahead of print.ABSTRACTTo explore the pathogenic mechanism of Salmonella Enteritidis (SE) infection in chicks and the regulatory role of Faecalibacterium, we established a chick SE infection model, systematically analyzing intestinal damage, systemic inflammation, and cecal microbial community changes. Focusing on the differentially abundant Faecalibacterium, we elucidated its regulatory mechanism via metagenomics, transcriptomics, and serum metabolomics. Results showed that SE successfully colonized the chick cecum, causing significant reductions in the thickness of the intestinal mucosal and muscular layers, a decrease in gland depth, and a loss of goblet cells. Concurrently, serum levels of IgA and IL-6 were markedly elevated, indicating the induction of systemic inflammatory responses and severe intestinal damage. Microbiome analysis revealed SE significantly altered cecal microbiota β-diversity, increased Actinobacteria abundance, and decreased the abundance of beneficial bacterial families (Lachnospiraceae and Oscillospiraceae) and the key beneficial genus Faecalibacterium. Functional prediction indicated microbial function remodeling towards enhanced pathogen colonization and pro-inflammation. β-diversity analysis of Faecalibacterium gene set showed clear separation between the Ctrl and SE groups in two-dimensional space: the control group was enriched in immune-related pathways such as Th17 cell differentiation and IL-17 signaling pathway, while the infected group was enriched in pathways related to Salmonella infection and pathogenic Escherichia coli infection. Validation in uninfected chicks showed High_ Faecalibacterium abundance was associated with lower serum IL-6, IL-8, IFN-γ and distinct gene expression profiles. Differentially expressed genes (DEGs) were enriched in immune regulation pathways such as cytokine-cytokine receptor interaction, NOD-like receptor signaling pathway, and intestinal immune network for IgA. LASSO regression screening identified 16 key associated genes including TM4SF4 and FABP4. Serum metabolomics showed distinct metabolic profiles between High_ and Low_ Faecalibacterium abundance groups, with 26 differential metabolites; N-(2,4-dinitrophenyl) ethylenediamine and Val-Gly-Phe (AUC > 0.8) were potential biomarkers. In conclusion, SE induces pathogenesis by damaging intestinal barrier, triggering inflammation, and disrupting cecal microbiota. Faecalibacterium enhances chick resistance to SE via regulating immune and metabolic homeostasis, providing a basis for avian salmonellosis microecological control.PMID:42623770 | DOI:10.1016/j.psj.2026.107550