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Novel Genes and Metabolite Trends in Bifidobacterium longum ssp. infantis Bi-26 Involved in Metabolism of Human Milk Oligosaccharide 2’-fucosyllactose

ABSTRACT: Novel Genes and Metabolite Trends in Bifidobacterium longum ssp. infantis Bi-26 Involved in Metabolism of Human Milk Oligosaccharide 2’-fucosyllactose

PROVIDER: PRJNA504863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8179920.fastq.gz	Fastqsanger.gz
	SRR8179921.fastq.gz	Fastqsanger.gz
	SRR8179922.fastq.gz	Fastqsanger.gz
	SRR8179923.fastq.gz	Fastqsanger.gz
	SRR8179914.fastq.gz	Fastqsanger.gz

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Novel Genes and Metabolite Trends in Bifidobacterium longum ssp. infantis Bi-26 Involved in Metabolism of Human Milk Oligosaccharide 2’-fucosyllactose

Project description:Human milk oligosaccharides (HMOs) function as prebiotics for beneficial bacteria in the developing gut, often dominated by Bifidobacterium spp. To understand the relationship between Bifidobacterium utilizing HMOs and how the metabolites that are produced could affect the host, we analyzed the metabolism of HMO 2’-fucosyllactose (2’-FL) in Bifidobacterium longum ssp. infantis Bi-26. RNA-seq and metabolite analysis (NMR/GCMS) was performed on samples at early (A600=0.25), mid-log (0.5-0.7) and late-log phases (1.0-2.0) of growth. Transcriptomic analysis revealed many gene clusters including three novel ABC-type sugar transport clusters to be upregulated in Bi-26 involved in processing of 2’-FL along with metabolism of its monomers glucose, fucose and galactose. Metabolite data confirmed the production of formate, acetate, 1,2-propanediol, lactate and cleaving of fucose from 2’-FL. The formation of acetate, formate, and lactate showed how the cell uses metabolites during fermentation to produce higher levels of ATP (mid-log compared to other stages) or generate cofactors to balance redox. We concluded 2’-FL metabolism is a complex process involving gene clusters throughout the genome producing more metabolites compared to lactose. These results provide valuable insight on the mode-of-action of 2’-FL utilization by Bifidobacterium longum ssp. infantis Bi-26.

2019-04-23 | GSE122350 | GEO

Strain-specific strategies of 2′-fucosyllactose, 3-fucosyllactose, and difucosyllactose assimilation by Bifidobacterium longum subsp. infantis Bi-26 and ATCC 15697

2020-06-07 | GSE151933 | GEO

Strain-Specific Strategies of Human Milk Oligosaccharide 2′-Fucosyllactose, 3-Fucosyllactose, and Difucosyllactose Assimilation by Bifidobacterium longum subsp. infantis Strains Bi-26 and ATCC 15697

Project description:Strain-Specific Strategies of Human Milk Oligosaccharide 2′-Fucosyllactose, 3-Fucosyllactose, and Difucosyllactose Assimilation by Bifidobacterium longum subsp. infantis Strains Bi-26 and ATCC 15697

| PRJNA637762 | ENA

Bifidobacterium infantis metabolizes 2´fucosyllactose-derived and free fucose through a common catabolic pathway resulting in 1,2-propanediol secretion

Project description:Human milk oligosaccharides (HMOs) enrich beneficial bifidobacteria in the infant gut microbiome which produce molecules that impact development and physiology. 2´fucosyllactose (2´FL) is a highly abundant fucosylated HMO which is utilized by Bifidobacterium longum subsp. infantis, despite limited scientific understanding of the underlying mechanism. Moreover, there is not a current consensus on whether free fucose could be metabolized when not incorporated in a larger oligosaccharide structure. Based on metabolic and genomic analyses, we hypothesize that B. infantis catabolizes both free fucose and fucosyl oligosaccharide residues to produce 1,2-propanediol (1,2-PD). Accordingly, systems-level approaches including transcriptomics and proteomics support this metabolic path. Co-fermentation of fucose and limiting lactose or glucose was found to promote significantly higher biomass and 1,2-PD concentrations than individual substrates, suggesting a synergistic effect. In addition, and during growth on 2´FL, B. infantis achieves significantly higher biomass corresponding to increased 1,2-PD. These findings support a singular fucose catabolic pathway in B. infantis that is active on both free and HMO-derived fucose and intimately linked with central metabolism. The impact of fucose and 2´FL metabolism on B. infantis physiology provides insight into the role of fucosylated HMOs in influencing host- and microbe-microbe interactions within the infant gut microbiome.

2020-10-08 | GSE159189 | GEO

The human milk oligosaccharide 2’-fucosyllactose alleviates liver steatosis and associated gut permeability, ER stress and insulin resistance by reducing hepatic diacylglycerols in obese Ldlr-/-.Leiden mice

Project description:Abstract: - Non-alcoholic fatty liver disease (NAFLD) is a complex multifactorial disorder that is associated with gut dysbiosis, enhanced gut permeability, adiposity and insulin resistance. Prebiotics such as human milk oligosaccharide 2’-fucosyllactose are thought to primarily improve gut health and it is uncertain whether they would affect more distant organs. This study investigates whether 2’-fucosyllactose can alleviate NAFLD development in manifest obesity. Obese hyperinsulinemic Ldlr-/-.Leiden mice, after an 8 week run-in on HFD, were treated with 2’-fucosyllactose by oral gavage until week 28 and compared to HFD-vehicle controls. 2’-fucosyllactose did not affect food intake, body weight, total fat mass or plasma lipids. 2’-fucosyllactose altered the fecal microbiota composition which was paralleled by a suppression of HFD-induced gut permeability at t=12 weeks. 2’-fucosyllactose significantly attenuated the development of NAFLD by reducing microvesicular steatosis. These hepatoprotective effects were supported by functional transcriptome analyses showing that 2’-fucosyllactose activated ACOX1 (involved in lipid catabolism), while deactivating SREBF1 (involved in lipogenesis). Furthermore, 2’-fucosyllactose suppressed ATF4, ATF6, ERN1, and NUPR1 all of which participate in ER stress. 2’-fucosyllactose reduced fasting insulin concentrations and HOMA-IR, which was corroborated by decreased intrahepatic diacylglycerols. - In conclusion, long-term prebiotic treatment with 2’-fucosyllactose can counteract the detrimental effects of HFD on gut dysbiosis and gut permeability and attenuates the development of liver steatosis. The observed reduction in intrahepatic diacylglycerols provides a mechanistic rationale for the improvement of hyperinsulinemia and supports the use of 2’-fucosyllactose to correct dysmetabolism and insulin resistance.

2022-05-24 | GSE195862 | GEO

Bifidobacterium infantis metabolizes 2´fucosyllactose-derived and free fucose through a common catabolic pathway resulting in 1,2-propanediol secretion

Project description:Human milk oligosaccharides (HMOs) are highly diverse complex carbohydrates secreted in human milk. HMOs are indigestible by the infant and instead are metabolized by bifidobacteria in the infant gut microbiome to produce molecules that promote infant health and development. 2´fucosyllactose (2´FL) is an abundant HMO and is utilized by Bifidobacterium longum subsp. infantis, a predominant member of the infant gut microbiome. Currently, there is not a scientific consensus on how or if bifidobacteria metabolize the fucose portion of 2´FL or free fucose. This proteomic analysis was conducted in order to characterize the metabolic pathway by which B. infantis utilizes fucose.

2021-03-17 | PXD021868 | Pride

Bifidobacterium kashiwanohense expresses fucosidases necessary for fucosyllactose utilisation as an adaptation to the infant gut environment

Project description:Bifidobacteria dominate the composition of the neonatal gut microbiota in the first number of weeks following birth. A number of species in particular are found with a significantly higher frequency in the microbiome of breastfed infants, owing to their ability to rely on Human Milk Oligosacchraides (HMOs) as their sole carbohydrate substrate; namely B. bifidum, B. longum spp. infantis and B. breve. Bifidobacterium kashiwanohense is a species that has been isolated previously only from the faeces of infants, but extremely infrequently at that. Relatively little is currently known about the species itself, let alone the metabolic pathways that allow it to successfully establish a population in the infant gut. We have isolated a novel strain of B. kashiwanohense from the faeces of a breastfed infant on the basis of its ability to utilise the HMO component fucosyllactose as its sole carbohydrate source. In this study, we read and annotate the full genome sequence of this novel strain, and use the data obtained to direct our further experimental analysis of fucosyllactose metabolism in B. kashiwanohense. Using transcriptomic and growth analysis results, we identify the genes responsible for B. kashiwanohense to utilise fucosyllactose, and employ a combination of cloning, in vitro hydrolysis assays, and further, recombinant transcriptomic and growth assays to elucidate the pathway for fucosyllactose metabolism in B. kashiwanohense, as well as revealing insight into fucosyllactose and fucose metabolism in Bifidobacteria as whole.

2019-11-12 | GSE107439 | GEO

Bifidobacterium longum subsp. infantis (B. infantis) strain dependent utilization of human milk oligosaccharides

Project description:Bifidobacterium longum subsp. infantis (B. infantis) colonizes the infant gut microbiome with a 43-kb gene cluster that enables human milk oligosaccharide (HMO) utilization. Although there is relative genomic homogeneity in this regard, previous observations suggest that B. infantis strains may differ in their utilization phenotype. To test this hypothesis, a panel of B. infantis strains were evaluated for their ability to utilize pooled HMOs to yield differential phenotypes including biomass accumulation, HMO consumption glycoprofile, end-product secretion, and global transcriptomes. Two strains (ATCC 15697 and UMA301) efficiently consumed several HMO isomers/anomers that exhibit degrees of polymerization (DP) ³ 4. These same strains partially consumed the smaller DP HMOs including fucosyllactose and lactodifucotetraose isomers/anomers. In contrast, UMA299 efficiently utilized fucosylated small molecular weight HMOs (DP<4), and accumulated greater biomass on purified 2´FL with significantly higher 1,2-propanediol production. This study identifies several strain-dependent features in HMO utilization phenotypes that are consistent with metabolic variation within a bifidobacterial-dominated infant-gut microbiome.

2020-12-30 | GSE164005 | GEO

The human milk oligosaccharide 2’-fucosyllactose protects against high-fat diet induced obesity by changing intestinal mucus production, composition and degradation linked to changes in gut microbiota and fecal proteome profiles in mice

Project description:The aim of this study was to decipher the mechanisms by which the major human milk oligosaccharide (HMO), 2’-fucosyllactose (2’FL), can affect body weight and fat mass gain upon high-fat diet (HFD) feeding in mice. In particular, we wanted to elucidate whether 2’FL metabolic effects are linked with changes in intestinal mucus production and secretion, mucin glycosylation and degradation, as well as with the modulation of the gut microbiota, fecal proteome and endocannabinoid (eCB) system.

2025-05-06 | PXD049406 | Pride

Bifidobacteria infantis and human milk oligosaccharides have independent effects on immune response and amino acid metabolism in germ-free mouse models

Project description:Early-life microbial colonization is essential for gut and immune development. Human milk oligosaccharides (HMO) support the growth of Bifidobacterium infantis (BI), a keystone infant species. Herein, we studied the individual and combined effects of BI and HMO on immune and colon transcriptomes, and the serum metabolome. Germ-free mice were randomly assigned to four groups [10-14/group: HMO, BI, BI+HMO and control (no HMO or BI)]. HMO and BI+HMO groups received 5 mg/d each of 2′-fucosyllactose, lacto-N-tetraose and 3′-sialyllactose for 14 d. BI and BI+HMO received B. infantis ATCC 15697 (1x10^9 CFU/d) on days 1, 4, and 9. Mono-colonization with BI increased monocytes, macrophages, B cells, CD4+ T cells, and Treg cells in mesenteric lymph nodes (MLN) relative to control. In the spleen, BI alone increased B cells, dendritic cells, Th17 cells, and ILC3 cells, and enriched serum amino acid metabolism pathways. Additionally, BI influenced colonocyte gene expression, and modulated serum metabolites regulating circadian rhythms. BI+HMO increased MLN Th17 cells and spleen monocytes compared to HMO alone. Collectively, the results of this study highlight the complex interplay between host-microbe-diet interactions and emphasize the importance of considering these interactions when designing strategies to modulate infant health during early life.

2026-06-01 | GSE310711 | GEO

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