Dataset Information

Microplastics Induce Damage to Cattle and Potential Health Risks Through Microbial Mediation: A Rumen Microbiota-Gut-Liver Axis Perspective_Rumen Fluid

ABSTRACT:

Microplastics pollution is prevalent in livestock environments, especially in ruminant feed. Exposure to microplastics can damage the gastrointestinal barrier, alter microbiota, and lead to organ damage. Despite its impact on cattle farming and potential human health risks, the effects of microplastics on cattle remain unexplored. This study investigates microplastic-induced toxicity through the rumen microbiota-gut-liver axis in beef cattle. We found that Microplastic exposure reduced body weight gain and liver development, induced pathological changes in the liver, increased lipopolysaccharide (LPS) levels in both blood and muscle, and triggered systemic inflammation, particularly affecting the liver. Alterations in rumen microbiota and metabolites were associated with liver inflammation. Furthermore, microplastics damaged the rumen, jejunum, and colon barriers, resulting in microbial dysbiosis, metabolic disorders, and activation of LPS synthesis pathways. Metabolomics of rumen fluid identified key metabolites-including 4-Fluoro-3-phenoxybenzoic acid and Isovalerylglutamic acid, which correlated with inflammatory markers (LPS, TNF-α, and IL-6). Transcriptomic analysis further corroborated inflammation in blood and liver, revealing activation of NF-κB pathway primarily via Toll-like receptor 4 (TLR4), which inhibited hepatocyte proliferation and promoted apoptosis.

Collectively, this study reveals that microplastics impair cattle liver function via the rumen microbiota-gut-liver axis. Microplastics disrupt the rumen microbiota, activate the LPS synthesis, and damage the intestinal barrier, allowing LPS to enter the bloodstream and subsequent liver damage. Additionally, LPS will also remain in the muscles, which to some extent exacerbates the risk of LPS in meat products to human health. Reducing the use of plastic products in animal husbandry and modulation of the rumen microbiota may provide a potential strategy to alleviate microplastic-induced hepatotoxicity.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS12959 | MetaboLights | 2025-09-08

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS12959_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS12959_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS12959_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS12959_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:<p> Microplastics pollution is prevalent in livestock environments, especially in ruminant feed. Exposure to microplastics can damage the gastrointestinal barrier, alter microbiota, and lead to organ damage. Despite its impact on cattle farming and potential human health risks, the effects of microplastics on cattle remain unexplored. This study investigates microplastic-induced toxicity through the rumen microbiota-gut-liver axis in beef cattle. We found that Microplastic exposure reduced body weight gain and liver development, induced pathological changes in the liver, increased lipopolysaccharide (LPS) levels in both blood and muscle, and triggered systemic inflammation, particularly affecting the liver. Alterations in rumen microbiota and metabolites were associated with liver inflammation. Furthermore, microplastics damaged the rumen, jejunum, and colon barriers, resulting in microbial dysbiosis, metabolic disorders, and activation of LPS synthesis pathways. Metabolomics of rumen fluid identified key metabolites-including 4-Fluoro-3-phenoxybenzoic acid and Isovalerylglutamic acid, which correlated with inflammatory markers (LPS, TNF-α, and IL-6). Transcriptomic analysis further corroborated inflammation in blood and liver, revealing activation of NF-κB pathway primarily via Toll-like receptor 4 (TLR4), which inhibited hepatocyte proliferation and promoted apoptosis.</p><p> Collectively, this study reveals that microplastics impair cattle liver function via the rumen microbiota-gut-liver axis. Microplastics disrupt the rumen microbiota, activate the LPS synthesis, and damage the intestinal barrier, allowing LPS to enter the bloodstream and subsequent liver damage. Additionally, LPS will also remain in the muscles, which to some extent exacerbates the risk of LPS in meat products to human health. Reducing the use of plastic products in animal husbandry and modulation of the rumen microbiota may provide a potential strategy to alleviate microplastic-induced hepatotoxicity.  </p>

Project description:In dairy cows, administration of high dosages of niacin (NA) was found to cause anti-lipolytic effects, which are mediated by the NA receptor hydroxyl-carboxylic acid receptor 2 (HCAR2) in white adipose tissue (WAT), and thereby to an altered hepatic lipid metabolism. However, almost no attention has been paid to possible direct effects of NA in cattle liver, despite showing that HCAR2 is expressed also in the liver of cattle and is even more abundant than in WAT. Due to this, we hypothesized that feeding of rumen-protected NA to dairy cows influences critical metabolic and/or signaling pathways in the liver through inducing changes in the hepatic transcriptome. In order to identify these pathways, we applied genome-wide transcript profiling in liver biopsies obtained at 1 wk postpartum (p.p.) from dairy cows of a recent study (Zeitz et al., 2018) which were fed a total mixed ration without (control group) or with rumen-protected NA from 21 d before calving until 3 wk p.p. Hepatic transcript profiling revealed that a total of 487 transcripts were differentially expressed [filter criteria fold change (FC) > 1.2 or FC < -1.2 and P < 0.05] in the liver at 1 wk p.p. between cows fed NA and control cows. Substantially more transcripts were down-regulated (n = 338), while only 149 transcripts were up-regulated by NA in the liver of cows. Gene set enrichment analysis (GSEA) for the up-regulated transcripts revealed that the most enriched gene ontology (GO) biological process terms were exclusively related to immune processes, such as leukocyte differentiation, immune system process, leukocyte differentiation, activation of immune response and acute inflammatory response. In line with this, the plasma concentration of the acute phase protein haptoglobin tended to be increased in dairy cows fed rumen-protected NA compared to control cows (P < 0.1). GSEA of the down-regulated transcripts showed that the most enriched biological process terms were related to metabolic processes, such as cellular metabolic process, small molecule metabolic process, lipid catabolic process, organic cyclic compound metabolic process, small molecule biosynthetic process and cellular lipid catabolic process. In conclusion, hepatic transcriptome analysis shows that rumen-protected NA induces genes which are involved mainly in immune processes including acute phase response and stress response in dairy cows at wk 1 p.p. These findings indicate that supplementation of rumen-protected NA to dairy cows in the periparturient period may induce or amplify the systemic inflammation-like condition which is typically observed in the liver of high-yielding dairy cows in the p.p. period.

Dataset Information

Microplastics Induce Damage to Cattle and Potential Health Risks Through Microbial Mediation: A Rumen Microbiota-Gut-Liver Axis Perspective_Rumen Fluid

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