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Heat stress exposure cause alterations in intestinal microbiota, transcriptome, and metabolome of broilers
Summary
Researchers found that heat stress in broilers significantly reduced growth performance while disrupting intestinal microbiota, increasing harmful Proteobacteria and decreasing beneficial Firmicutes. Multi-omics analysis revealed that purine metabolism is a key co-participating pathway linking gene expression, metabolite changes, and microbial shifts caused by heat-induced oxidative stress.
The results indicate that heat stress significantly reduced the average daily gain and body weight of broilers (value of p < 0.05). Transcriptome KEGG enrichment showed that the differential genes were mainly enriched in the NF-kB signaling pathway. Metabolomics results showed that KEGG enrichment showed that the differential metabolites were mainly enriched in the mTOR signaling pathway. 16S rDNA amplicon sequencing results indicated that heat stress increased the relative abundance of Proteobacteria decreased the relative abundance of Firmicutes. Multi-omics analysis showed that the co-participating pathway of differential genes, metabolites and microorganisms KEGG enrichment was purine metabolism. Pearson correlation analysis found that ornithine was positively correlated with SULT1C3, GSTT1L and g_Lactobacillus, and negatively correlated with CALB1. PE was negatively correlated with CALB1 and CHAC1, and positively with g_Alistipes. In conclusion, heat stress can generate large amounts of reactive oxygen and increase the types of harmful bacteria, reduce intestinal nutrient absorption and antioxidant capacity, and thereby damage intestinal health and immune function, and reduce growth performance indicators. This biological process is manifested in the complex regulation, providing a foundational theoretical basis for solving the problem of heat stress.