Quantification and characterization of mouse and human tissue-resident microbiota by qPCR and 16S sequencing

Yao, Bingqing; Fu, Aikun; Li, Hang; Jiang, Chuhan; Li, Nan; Dong, Tingting

doi:10.1016/j.xpro.2022.101765

Cited by 4 publications

(1 citation statement)

References 20 publications

(30 reference statements)

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“…The bacterial genomic DNA was extracted from the cecum, and feces in the colon of the DB group by using a QiAamp PowerFecal Pro DNA kit (Qiagen, USA). 73 The V3-V4 region of the 16S rRNA gene was amplified by following the manufacturer’s instructions. 74 The raw sequences were preprocessed and quality-controlled using QIIME 2 with default parameters of the Illumina MiSeq System.…”

Section: Methodsmentioning

confidence: 99%

B. longum CKD1 enhances the efficacy of anti-diabetic medicines through upregulation of IL- 22 response in type 2 diabetic mice

Kim,

Kil,

Lee

et al. 2024

Gut Microbes

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The gut microbiota plays a pivotal role in metabolic disorders, notably type 2 diabetes mellitus (T2DM). In this study, we investigated the synergistic potential of combining the effects of Bifidobacterium longum NBM7–1 (CKD1) with anti-diabetic medicines, Lobeglitazone Ⓡ (LO), Sitagliptin Ⓡ (SI), and Metformin Ⓡ (Met), to alleviate hyperglycemia in a diabetic mouse model. CKD1 effectively mitigated insulin resistance, hepatic steatosis, and enhanced pancreatic β-cell function, as well as fortifying gut-tight junction integrity. In the same way, SI-CKD1 and Met- CKD1 synergistically improved insulin sensitivity and prevented hepatic steatosis, as evidenced by the modulation of key genes associated with insulin signaling, β-oxidation, gluconeogenesis, adipogenesis, and inflammation by qRT-PCR. The comprehensive impact on modulating gut microbiota composition was observed, particularly when combined with Metformin Ⓡ . This combination induced an increase in the abundance of Rikenellaceae and Alistipes related negatively to the T2DM incidence while reducing the causative species of Cryptosporangium, Staphylococcaceae , and Muribaculaceae . These alterations intervene in gut microbiota metabolites to modulate the level of butyrate, indole-3-acetic acid, propionate, and inflammatory cytokines and to activate the IL-22 pathway. However, it is meaningful that the combination of B. longum NBM7–1(CKD1) reduced the medicines’ dose to the level of the maximal inhibitory concentrations (IC50). This study advances our understanding of the intricate relationship between gut microbiota and metabolic disorders. We expect this study to contribute to developing a prospective therapeutic strategy modulating the gut microbiota.

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Section: Methodsmentioning

confidence: 99%

B. longum CKD1 enhances the efficacy of anti-diabetic medicines through upregulation of IL- 22 response in type 2 diabetic mice

Kim,

Kil,

Lee

et al. 2024

Gut Microbes

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Evaluation of synbiotic combinations of commercial probiotic strains with different prebiotics in in vitro and ex vivo human gut microcosm model

Raval,

Archana

2024

Arch Microbiol

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ACOD1 deficiency offers protection in a mouse model of diet-induced obesity by maintaining a healthy gut microbiota

Eberhart,

Stanley,

Ricci

et al. 2024

Cell Death Dis

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Aconitate decarboxylase 1 (ACOD1) is the enzyme synthesizing itaconate, an immuno-regulatory metabolite tuning host-pathogen interactions. Such functions are achieved by affecting metabolic pathways regulating inflammation and microbe survival. However, at the whole-body level, metabolic roles of itaconate remain largely unresolved. By using multiomics-integrated approaches, here we show that ACOD1 responds to high-fat diet consumption in mice by promoting gut microbiota alterations supporting metabolic disease. Genetic disruption of itaconate biosynthesis protects mice against obesity, alterations in glucose homeostasis and liver metabolic dysfunctions by decreasing meta-inflammatory responses to dietary lipid overload. Mechanistically, fecal metagenomics and microbiota transplantation experiments demonstrate such effects are dependent on an amelioration of the intestinal ecosystem composition, skewed by high-fat diet feeding towards obesogenic phenotype. In particular, unbiased fecal microbiota profiling and axenic culture experiments point towards a primary role for itaconate in inhibiting growth of Bacteroidaceae and Bacteroides, family and genus of Bacteroidetes phylum, the major gut microbial taxon associated with metabolic health. Specularly to the effects imposed by Acod1 deficiency on fecal microbiota, oral itaconate consumption enhances diet-induced gut dysbiosis and associated obesogenic responses in mice. Unveiling an unrecognized role of itaconate, either endogenously produced or exogenously administered, in supporting microbiota alterations underlying diet-induced obesity in mice, our study points ACOD1 as a target against inflammatory consequences of overnutrition.

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Quantification and characterization of mouse and human tissue-resident microbiota by qPCR and 16S sequencing

Cited by 4 publications

References 20 publications

B. longum CKD1 enhances the efficacy of anti-diabetic medicines through upregulation of IL- 22 response in type 2 diabetic mice

B. longum CKD1 enhances the efficacy of anti-diabetic medicines through upregulation of IL- 22 response in type 2 diabetic mice

Evaluation of synbiotic combinations of commercial probiotic strains with different prebiotics in in vitro and ex vivo human gut microcosm model

ACOD1 deficiency offers protection in a mouse model of diet-induced obesity by maintaining a healthy gut microbiota

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