Genetic and Probiotic Characteristics of Urolithin A Producing Enterococcus faecium FUA027

Xia, Mengjie; Mu, Shuting; Fang, Yiwu; Zhang, Xiaomeng; Yang, Guang; Hou, Xiaoyue; He, Fuxiang; Zhao, Yaling; Huang, Yichen; Zhang, Wei; Shen, Juan; Liu, Shu

doi:10.3390/foods12051021

Cited by 11 publications

(5 citation statements)

References 46 publications

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“…A maximum concentration of 7.3 µmol/L of urolithin A was produced after 50 h of anaerobic culture in an ABB medium supplemented with 20 µmol/L EA and 0.005% L-cysteine. Other bacteria, such as Enterococcus faecium FUA029 and Lactococcus garviae FUA009, were also implicated in the production of urolithin A under similar growth conditions [31][32][33]. Urolithin A and B from EA were produced by Bifidobacterium pseudocatenulatum INIA P815 [34].…”

Section: Fermentation 0 H 24 H 48 H 72 H S Thermophilusmentioning

confidence: 99%

Fermentative Liberation and Transformation of Bioactive Compounds: Ellagic Acid from Nut Press Cake Ellagitannins

Brück,

Erismann,

Andlauer

2024

Applied Sciences

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Oil extracted from walnuts leaves behind large amounts of defatted press cake that still retains valuable nutrients. Solid state fermentation (SSF) is a promising method to liberate bioactive compounds from food by-products. Aspergillus oryzae, Rhizopus oligosporus, and Streptococcus thermophilus possess the necessary enzymes to utilize these nutrients from the walnut press cake (WPC) and convert walnut ellagitannins into ellagic acid and urolithins. This study conducted SSF with WPC to release ellagic acid from ellagitannins and form urolithins. The growth of the two filamentous fungi could be observed visually and the growth of Streptococcus thermophilus was confirmed by plate count technique. Extracts from fermented products were subjected to analysis using HPLC–DAD to measure the release of ellagic acid from ellagitannins. Additionally, a more sensitive UHPLC–MS method was employed to screen fermented samples for urolithin A. The ellagic acid content exhibited no perceptible change but was already present in the press cake before and after all fermentations. Urolithin A was undetectable, even with the more sensitive MS method. All studies showing urolithin A formation were conducted under anaerobic conditions. This might be a basic prerequisite for the transformation of ellagic acid to urolithins.

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Section: Fermentation 0 H 24 H 48 H 72 H S Thermophilusmentioning

confidence: 99%

Fermentative Liberation and Transformation of Bioactive Compounds: Ellagic Acid from Nut Press Cake Ellagitannins

Brück,

Erismann,

Andlauer

2024

Applied Sciences

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“…Strains converting EA to Uro-A are currently limited. Bifidobacterium pseudocatenulatum INIA P815, Lactococcus garvieae FUA009, and Enterococcus faecium FUA027 isolated from human feces can produce Uro-A from EA Enterocloster bolteae CEBAS S4A9 isolated from human feces converted Uro-C to Uro-A .…”

Section: Introductionmentioning

confidence: 99%

Improvement of Urolithin A Yield by In Vitro Cofermentation of Streptococcus thermophilus FUA329 with Human Gut Microbiota from Different Urolithin Metabotypes

Xia,

Hua,

Zhao

et al. 2024

J. Agric. Food Chem.

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Streptococcus thermophilus FUA329 converts ellagic acid (EA) to urolithin A (Uro-A), which is not autonomously converted by the gut microbiota to produce highly bioavailable and multibiologically active Uro-A in urolithin metabotype 0 (UM-0) populations. We consider that Streptococcus thermophilus FUA329 has the potential to be developed as a probiotic. Therefore, we utilized S. thermophilus FUA329 for in vitro cofermentation with gut microbiota. The results revealed that strain FUA329 increased the production of EA-converted Uro-A during in vitro cofermentation with the human gut microbiota of different urolithin metabotypes (UMs), with a significant increase in the production of Uro-A in the experimental group of UM-0. In addition, changes in the in vitro cofermentation microbial community were determined using high-throughput sequencing. Strain FUA329 modulated the structure and composition of the gut microbiota in different UMs, thereby significantly increasing the abundance of beneficial microbiota in the gut microbiota while decreasing the abundance of harmful microbiota. Of greatest interest was the significant increase in the abundance of Actinobacteria phylum after the cofermentation of strain FUA329 with UM-0 gut microbiota, which might be related to the significant increase in the production of Uro-A.

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“…Urolithins are produced in the gut following the microbiome-mediated transformation of the natural polyphenols ellagitannins (ETs) and ellagic acid (EA), which are present in dietary products, such as pomegranates, berries, and walnuts ( 15 – 25 ). Recently, in vitro culture studies have shown that Bifidobacterium pseudocatenulatum INIA P815 ( 26 ), Enterococcus faecium FUA027 ( 27 ), and Streptococcus thermophilus FUA329 ( 28 ) can metabolize ellagic acid to produce UroA. However, their role in UroA production in vivo has not yet been established.…”

Section: Introductionmentioning

confidence: 99%

The microbial metabolite urolithin A reduces Clostridioides difficile toxin expression and toxin-induced epithelial damage

Ghosh,

Erickson,

Chua

et al. 2024

mSystems

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Clostridioides difficile is a Gram-positive, anaerobic, spore-forming bacterium responsible for antibiotic-associated pseudomembranous colitis. Clostridioides difficile infection (CDI) symptoms can range from diarrhea to life-threatening colon damage. Toxins produced by C. difficile (TcdA and TcdB) cause intestinal epithelial injury and lead to severe gut barrier dysfunction, stem cell damage, and impaired regeneration of the gut epithelium. Current treatment options for intestinal repair are limited. In this study, we demonstrate that treatment with the microbial metabolite urolithin A (UroA) attenuates CDI-induced adverse effects on the colon epithelium in a preclinical model of CDI-induced colitis. Moreover, our analysis suggests that UroA treatment protects against C. difficile- induced inflammation, disruption of gut barrier integrity, and intestinal tight junction proteins in the colon of CDI mice. Importantly, UroA treatment significantly reduced the expression and release of toxins from C. difficile without inducing bacterial cell death. These results indicate the direct regulatory effects of UroA on bacterial gene regulation. Overall, our findings reveal a novel aspect of UroA activity, as it appears to act at both the bacterial and host levels to protect against CDI-induced colitis pathogenesis. This research sheds light on a promising avenue for the development of novel treatments for C. difficile infection. IMPORTANCE Therapy for Clostridioides difficile infections includes the use of antibiotics, immunosuppressors, and fecal microbiota transplantation. However, these treatments have several drawbacks, including the loss of colonization resistance, the promotion of autoimmune disorders, and the potential for unknown pathogens in donor samples. To date, the potential benefits of microbial metabolites in CDI-induced colitis have not been fully investigated. Here, we report for the first time that the microbial metabolite urolithin A has the potential to block toxin production from C. difficile and enhance gut barrier function to mitigate CDI-induced colitis.

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Genetic and Probiotic Characteristics of Urolithin A Producing Enterococcus faecium FUA027

Cited by 11 publications

References 46 publications

Fermentative Liberation and Transformation of Bioactive Compounds: Ellagic Acid from Nut Press Cake Ellagitannins

Fermentative Liberation and Transformation of Bioactive Compounds: Ellagic Acid from Nut Press Cake Ellagitannins

Improvement of Urolithin A Yield by In Vitro Cofermentation of Streptococcus thermophilus FUA329 with Human Gut Microbiota from Different Urolithin Metabotypes

The microbial metabolite urolithin A reduces Clostridioides difficile toxin expression and toxin-induced epithelial damage

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