Methyl-donor supplementation prevents intestinal colonization by Adherent-Invasive E. coli in a mouse model of Crohn’s disease

Gimier, Elodie; Chervy, Mélissa; Agus, Allison; Sivignon, Adeline; Billard, Elisabeth; Privat, Maud; Viala, Sandrine; Minet-Quinard, Régine; Buisson, A.; Vazeille, Emilie; Barnich, Nicolas; Denizot, Jérémy

doi:10.1038/s41598-020-69472-3

Cited by 10 publications

(11 citation statements)

References 63 publications

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“…FA is a kind of methyl-donor. A previous study found that methyl-donor supplemented diet prevents the colonization of intestinal E. coli in a mouse model of Crohn’s disease, which may be by influencing the DNA methylation level of CEACAM6 gene (a kind of cell adhesion molecule) [ 65 ]. Similarly, in mice, FA supplementation prevent Helicobacter-associated gastric cancer by increasing global DNA methylation [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptome sequencing analysis for the identification of stable lncRNAs associated with bovine Staphylococcus aureus mastitis

Tang

Dari

et al. 2021

J Animal Sci Biotechnol

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Background Staphylococcus aureus (S. aureus) mastitis is one of the most difficult diseases to treat in lactating dairy cows worldwide. S. aureus with different lineages leads to different host immune responses. Long non-coding RNAs (lncRNAs) are reported to be widely involved in the progress of inflammation. However, no research has identified stable lncRNAs among different S. aureus strain infections. In addition, folic acid (FA) can effectively reduce inflammation, and whether the inflammatory response caused by S. aureus can be reduced by FA remains to be explored. Methods lncRNA transcripts were identified from Holstein mammary gland tissues infected with different concentrations of S. aureus (in vivo) and mammary alveolar cells (Mac-T cells, in vitro) challenged with different S. aureus strains. Differentially expressed (DE) lncRNAs were evaluated, and stable DE lncRNAs were identified in vivo and in vitro. On the basis of the gene sequence conservation and function conservation across species, key lncRNAs with the function of potentially immune regulation were retained for further analysis. The function of FA on inflammation induced by S. aureus challenge was also investigated. Then, the association analysis between these keys lncRNA transcripts and hematological parameters (HPs) was carried out. Lastly, the knockdown and overexpression of the important lncRNA were performed to validate the gene function on the regulation of cell immune response. Results Linear regression analysis showed a significant correlation between the expression levels of lncRNA shared by mammary tissue and Mac-T cells (P < 0.001, R2 = 0.3517). lncRNAs PRANCR and TNK2–AS1 could be regarded as stable markers associated with bovine S. aureus mastitis. Several HPs could be influenced by SNPs around lncRNAs PRANCR and TNK2–AS1. The results of gene function validation showed PRANCR regulates the mRNA expression of SELPLG and ITGB2 within the S. aureus infection pathway and the Mac-T cells apoptosis. In addition, FA regulated the expression change of DE lncRNA involved in toxin metabolism and inflammation to fight against S. aureus infection. Conclusions The remarkable association between SNPs around these two lncRNAs and partial HP indicates the potentially important role of PRANCR and TNK2–AS1 in immune regulation. Stable DE lncRNAs PRANCR and TNK2–AS1 can be regarded as potential targets for the prevention of bovine S. aureus mastitis. FA supplementation can reduce the negative effect of S. aureus challenge by regulating the expression of lncRNAs.

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Section: Discussionmentioning

confidence: 99%

Transcriptome sequencing analysis for the identification of stable lncRNAs associated with bovine Staphylococcus aureus mastitis

Tang

Dari

et al. 2021

J Animal Sci Biotechnol

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“…However, a lack of methyl donors can affect the differentiation and barrier functions of the small intestine and increase the concentration of Hcy, which subsequently promotes oxidative stress and activates interrelated pro-inflammatory mechanisms, ultimately aggravating inflammatory bowel disease in rats ( 13 , 33 ). MET supplementation through the diet limits pathobiont colonization of the gut via inducing a specific intestinal micro-environment ( 11 ). When the harmful bacteria decrease, the beneficial bacteria may increase relatively.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, there is increasing evidence that microbiota-derived metabolites are key factors regulating animal metabolism, growth, and development ( 10 ). Maternal-MET supplementation induces a specific intestinal microenvironment, limiting pathobiont colonization [such as adherent-invasive Escherichia coli (AIEC)] of the offspring gut ( 11 ). Conversely, other studies report that maternal-MET supplementation or deficiency leads to an increase in the sensitivity to colitis in the offspring ( 12 , 13 ), suggesting the central role of MET in the intestinal microenvironment.…”

Section: Introductionmentioning

confidence: 99%

Methyl-Donor Micronutrient for Gestating Sows: Effects on Gut Microbiota and Metabolome in Offspring Piglets

Zou

et al. 2021

Front. Nutr.

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This study aimed to investigate the effects of maternal methyl-donor micronutrient supplementation during gestation on gut microbiota and the fecal metabolic profile in offspring piglets. Forty-three Duroc × Erhualian gilts were assigned to two dietary groups during gestation: control diet (CON) and CON diet supplemented with MET (folic acid, methionine, choline, vitamin B6, and vitamin B12). The body weights of offspring piglets were recorded at birth and weaning. Besides this, fresh fecal samples of offspring piglets were collected at 7, 14, and 21 days. The gut microbiota composition, metabolic profile, and short-chain fatty acid (SCFA) profiles in the fecal samples were determined using 16S rDNA sequencing, liquid chromatography-mass spectrometry metabolomics, and gas chromatography methods, respectively. The results showed that maternal methyl-donor micronutrient supplementation increased the microbiota diversity and uniformity in feces of offspring piglets as indicated by increased Shannon and Simpson indices at 7 days, and greater Simpson, ACE, Chao1 and observed species indices at 21 days. Specifically, at the phylum level, the relative abundance of Firmicutes and the Firmicutes to Bacteroidetes ratio were elevated by maternal treatment. At the genus level, the relative abundance of SCFA-producing Dialister, Megasphaera, and Turicibacter, and lactate-producing Sharpea as well as Akkermansia, Weissella, and Pediococcus were increased in the MET group. The metabolic analyses show that maternal methyl-donor micronutrient addition increased the concentrations of individual and total SCFAs of 21-day piglets and increased metabolism mainly involving amino acids, pyrimidine, and purine biosynthesis. Collectively, maternal methyl-donor micronutrient addition altered gut microbiota and the fecal metabolic profile, resulting in an improved weaning weight of offspring piglets.

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“…In a mouse model of Crohn's disease (CD), methyl-donor supplementation can prevent the intestinal colonization of adherent-invasive E. coli, showing beneficial effects on the inflammation. Furthermore, the serum folate concentration was found to be inversely correlated to fecal inflammatory markers in a cohort of CD [59]. MD supplementation during pregnancy increased the odds of colitis infection in offspring, and was found to be associated with persistent epigenetic and intestinal microbial changes [57].…”

Section: Factors Involved In the Progress Of Colitismentioning

confidence: 92%

Dissecting the Interplay Mechanism between Epigenetics and Gut Microbiota: Health Maintenance and Disease Prevention

Wang

Wan

et al. 2021

IJMS

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The gut microbiota exists throughout the full life cycle of the human body, and it has been proven to have extensive impacts on health and disease. Accumulating evidence demonstrates that the interplay between gut microbiota and host epigenetics plays a multifaceted role in health maintenance and disease prevention. Intestinal microflora, along with their metabolites, could regulate multiple epigenetic pathways; e.g., DNA methylation, miRNA, or histone modification. Moreover, epigenetic factors can serve as mediators to coordinate gut microbiota within the host. Aiming to dissect this interplay mechanism, the present review summarizes the research profile of gut microbiota and epigenetics in detail, and further interprets the biofunctions of this interplay, especially the regulation of intestinal inflammation, the improvement of metabolic disturbances, and the inhibition of colitis events. This review provides new insights into the interplay of epigenetics and gut microbiota, and attempts to reveal the mysteries of health maintenance and disease prevention from this new perspective.

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Methyl-donor supplementation prevents intestinal colonization by Adherent-Invasive E. coli in a mouse model of Crohn’s disease

Cited by 10 publications

References 63 publications

Transcriptome sequencing analysis for the identification of stable lncRNAs associated with bovine Staphylococcus aureus mastitis

Transcriptome sequencing analysis for the identification of stable lncRNAs associated with bovine Staphylococcus aureus mastitis

Methyl-Donor Micronutrient for Gestating Sows: Effects on Gut Microbiota and Metabolome in Offspring Piglets

Dissecting the Interplay Mechanism between Epigenetics and Gut Microbiota: Health Maintenance and Disease Prevention

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