Heat stress suppresses lactation through potential rumen-mammary communication mediated by extracellular vesicles: integrated analysis of microbiome, metabolome, and miRNA profiles.

backgroundHeat stress (HS) imposes significant physiological and economic challenges to dairy production, yet the integrative mechanisms linking rumen microbial dysbiosis, host metabolic disruption, and lactation suppression remain not yet fully understood. Emerging evidence suggests that extracellular vesicles (EVs) and their cargo, particularly microRNAs (miRNAs), may participate in systemic inter-organ communication under stress. This study aimed to elucidate how HS suppresses lactation through potential rumen-mammary communication mediated by EVs, using a comprehensive multi-omics approach.

resultsDairy cows exposed to HS exhibited elevated rectal temperatures and respiratory rates, accompanied by significant reductions in the yield of milk, milk fat and protein. Rumen fermentation was markedly impaired, with decreased pH, butyrate, and valerate proportions, and systemic inflammation was evidenced by increased pro-inflammatory cytokines and barrier dysfunction. Metagenomic profiling revealed that HS reshaped the rumen microbiome, significantly reducing the relative abundances of Prevotella, Bifidobacterium, and Lactobacillus species while enriching methanogenic and low-efficiency fermentative taxa. Functionally, HS enhanced microbial methane metabolism and suppressed carbohydrate degradation pathways, reducing the host's energy supply for milk synthesis. Metabolomic analyses supported this shift, with distinct metabolites significantly correlated with lactation performance. Notably, extracellular vesicle (EV)-derived miRNAs from both plasma and milk showed significant expression changes under HS conditions, predominantly targeting signaling pathways related to stress and immune responses, hormone regulation, and mammary gland development and function.

conclusionsThis study demonstrates that HS suppresses lactation through multi-level alterations in the rumen microbiome, metabolic homeostasis, and EV-derived miRNA signaling, collectively supporting the existence of a potential rumen-mammary communication axis. These findings offer novel insights into the pathogenesis of HS responses.