Metabolite-mediated crosstalk: unraveling the interactions between gut microbiota and host in fatty liver hemorrhagic syndrome of laying hens

TL;DR

This review explores how gut microbiota and host metabolites interact to cause fatty liver hemorrhagic syndrome in laying hens, similar to human liver disease.

Contribution

The paper highlights metabolite-mediated crosstalk between gut microbiota and host as a novel perspective for understanding FLHS pathogenesis.

Findings

Host-derived metabolites regulate gut microbiota structure and function via the gut-liver axis in FLHS.

Microbial metabolites influence hepatic lipid metabolism, inflammation, and oxidative stress in FLHS progression.

Key microbes like Bacteroides, Lactobacillus, and Akkermansia muciniphila are potential therapeutic targets for FLHS.

Abstract

Fatty liver hemorrhagic syndrome (FLHS) in laying hens is a metabolic disorder characterized by excessive hepatic lipid accumulation, inflammation, and hemorrhage, bearing pathological similarities to human non-alcoholic fatty liver disease. With the rise of intensive poultry farming, the incidence of FLHS has markedly increased, resulting in significant economic losses in the poultry industry. The gut microbiota plays a crucial role in host digestion, metabolism, and immune regulation, particularly in liver diseases. Gut microbiota and its metabolites influence liver health via the gut-liver axis. This review aims to explore metabolite-mediated interactions between the laying hens and the gut microbiota, elucidating their role in the pathogenesis of FLHS. Host-derived metabolites, such as lipids, bile acids, amino acids, and carbohydrates, regulate the structure and function of the gut microbiota through the gut-liver axis, playing a role in FLHS progression. Concurrently, microbial metabolites, including short-chain fatty acids, bile acids, and amino acid derivatives, influence hepatic lipid metabolism, inflammation, and oxidative stress, driving the development of FLHS. Key microbes, such as Bacteroides, Lactobacillus, and Akkermansia muciniphila, are considered potential therapeutic targets due to their involvement in metabolite production. By integrating multi-omics data and mechanistic studies, this review highlights the central role of host–gut microbiota communication in FLHS and provides a theoretical basis and research direction for the development of microbiota-based intervention strategies.

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