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The Crosstalk between Microbiota and Metabolites in AP Mice Based on Metagenomics and Untargeted Metabolomics

ABSTRACT:

BACKGROUND AND PURPOSE: The microbiota dysfunction aggravated the severity of acute pancreatitis (AP), but the relationship between microbiota dysfunction and metabolites alteration was not fully explained. This study aimed to explore the crosstalk between microbiota and metabolites in AP mice.

METHODS: Experimental AP models were established by caerulein for 7 times plus lipopolysaccharide (LPS) for once in C57/BL mice. To reveal systemic disturbance of AP, metagenomics and untargeted metabolomics were applied to reveal systemic disturbance of microbiota and metabolites in AP progress, respectively.

RESULTS: Gut microbiota from AP mice was mainly composed of Firmicutes, Bacteroidetes, Actinobacteria and Proteobacteria, and presented a 'core microbiota' characterized by an expansion in Proteobacteria as well as a decrease in Actinobacteria. Kyoto encyclopedia of genes and genomes (KEGG) analysis found that the significantly differential microbiota was involved in several signaling networks. Moreover, 872 metabolites were identified from untargeted metabolomics. Among them, lipids and lipid-like molecules were majorly affected. The integrated analysis of metagenomics and metabolomics showed that acetate kinase (Acka) was associated with various gut microbiota, including Alistipes, Butyricimonas and Lactobacillus. Particularly, Acka was tightly correlated with the metabolite daphnoretin. Besides, the functional gene of O-acetyl-L-serine sulfhydrylase (Cysk) was correlated with Alistipes, Jeotgalicoccus and Lactobacillus, and which was associated with metabolites of bufalin and Phlorobenzophenone.

CONCLUSION: Our study uncovered the relationship between gut microbiota and metabolites during AP, especially the Lactobacillus, Alistipes and Butyricimonas associated functional genes (Acka and Cysk) was tightly correlated to anti-inflammation and anti-tumor metabolites (daphnoretin and bufalin).

INSTRUMENT(S): Liquid Chromatography MS - alternating - hilic

SUBMITTER: Qi Zhou

PROVIDER: MTBLS6831 | MetaboLights | 2023-08-10

REPOSITORIES: MetaboLights

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Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.

Project description:Background and aims. The etiopathology of inflammatory bowel diseases is still poorly understood. To date, only few little data are available on the microbiota composition in ulcerative colitis (UC), representing a major subform of inflammatory bowel diseases. Currently, one of the main challenges is to unravel the interactions between genetics and environmental factors in the onset or during the progression and maintenance of the disease. The aim of the present study was to analyse twin pairs discordant for UC for both gut microbiota dysbiosis and host expression profiles at a mucosal level and to get insight into the functional genomic crosstalk between microbiota and mucosal epithelium in vivo. Methods. Biopsies were sampled from the sigmoid colon of both healthy and diseased siblings from UC discordant twin pairs but also from healthy twins. Microbiota profiles were assessed by 16S rDNA libraries while mRNA expression profiles were analysed from the same volunteers using Affymetrix microarrays. Results. UC patients showed a dysbiotic microbiota with lower diversity and more species belonging to Actinobacteria and Proteobacteria phyla. On the contrary, their healthy siblingsM-bM-^@M-^Y microbiota contained more bacteria from the Lachnospiracea and Ruminococcaceae family than did healthy individuals . Sixty-three host transcripts significantly correlated with bacterial genera in healthy individuals whereas only 43 and 32 correlated with bacteria in healthy and UC siblings from discordant pairs, respectively. Several transcripts related to oxidative and immune responses were differentially expressed between unaffected and UC siblings. Conclusion. A loss of crosstalk between gut microbiota and host was highlighted in UC patients. This defect was also striking in healthy siblings from discordant pairs, as was the lower biodiversity within the microbiota. Our results suggest disease-relevant interactions between host transcriptome and microbiota. Moreover, unusual aerobic bacteria were noticed in UC mucosal microbiota, whereas healthy siblings from discordant pairs had higher percentages of potentially beneficialusual commensal bacterial species. Paired samples (twins) were analyzed to obtain data independent of genetic variation

			Action	DRS
	MTBLS6831	Other
	FILES	Other
	a_MTBLS6831_LC-MS_alternating_hilic_metabolite_profiling.txt	Txt
	files-all.json	Other
	i_Investigation.txt	Txt

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The Crosstalk between Microbiota and Metabolites in AP Mice Based on Metagenomics and Untargeted Metabolomics

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