We are analyzing https://link.springer.com/article/10.1186/s12866-016-0625-7.

Title:
Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice | BMC Microbiology
Description:
Background The constitutive inflammation that characterizes advanced age is termed inflamm-aging. This process is associated with age-related changes to immune homeostasis and gut microbiota. We investigated the relationship between aging and gut microbiota lipopolysaccharide (LPS)-inducible inflammation. Results A taxonomy-based analysis showed that aging resulted in increased prevalence of the phyla Firmicutes and Actinobacteria and a reduced prevalence of Bacteroidetes and Tenericutes, resulting in an increase in the Firmicutes to Bacteroidetes ratio. The levels of plasmatic and fecal lipopolysaccharides were higher in aged mice. Aging induced the expression of p16 and the activation of nuclear factor-kappa B (NF-κB) in the colon of aged mice. Interestingly, the expression level of sterile α-motif domain- and HD domain-containing protein 1 (SAMHD1) in the colon was higher in aged mice than in young mice, while cyclin-dependent kinase-2 and cyclin E levels were lower in aged mice than in young mice. The lipopolysaccharide fraction of fecal lysates (LFL) from young or aged mice increased p16 and SAMHD1 expression and NF-κB activation in peritoneal macrophages from wild-type mice, in a TLR4-dependent manner. However, LFLs did not induce NF-κB activation and SAMHD1 expression in peritoneal macrophages from TLR4-deificent mice, whereas they significantly induced p16 expression. Nevertheless, p16 expression was induced more potently in macrophages from WT mice than in macrophages from TLR4-deficient mice. Conclusion Aging increased p16 and SAMHD1 expression, gut microbiota LPS production, and NF-κB activation; thereby, signifying that gut microbiota LPS may accelerate inflamm-aging and SAMHD1 may be an inflamm-aging marker.
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Keywords {🔍}

mice, pubmed, microbiota, gut, young, article, aged, expression, samhd, google, scholar, aging, levels, macrophages, cas, lps, peritoneal, inflammation, fecal, central, composition, inflammaging, kim, firmicutes, cell, fig, increased, nfκb, increase, activation, analysis, bacteroidetes, cells, phylum, data, induced, inflammatory, endotoxin, age, elderly, shown, samples, full, results, protein, cyclin, dna, study, table, reported,

Topics {✒️}

taxonomy-based analysis showed lps-tlr4-dependent signal pathway dong-hyun kim tlr4-deficient c57bl/10scnj mice 16s rrna-based probes g1/s-specific regulators article download pdf aicardi-goutieres syndrome gene sterile α-motif domain dgtp-regulated deoxynucleotide triphosphohydrolase stem-cell ageing modified cyclin-dependent kinases cdk4 putative gtp-binding protein male c57bl/6j mice samhd1-interacting cellular proteins c-reactive protein increase exhibit anti-inflammatory effects gut microbiota-induced endotoxemia induce nf-κb activation nf-κb activation slightly gut microbiota lipopolysaccharide ameliorates experimental colitis lps-binding proteins increase full access cyclin a2/cdk1 regulates high-fat diet 16s rrna abundance privacy choices/manage cookies national research foundation tlr4 signaling pathway lipopolysaccharide-binding protein cellular proteins interacting body weight gain tlr4-dependent manner article kim cyclin-dependent kinase-2 kyung hee university creative commons license regulates cell proliferation disrupt gut microbiota nf-κb activation gut microbiota lps termed inflamm-aging accelerate inflamm-aging termed “inflamm-aging” called “inflamm-aging” [21] inflamm-aging condition anti-inflammatory networks cell-cycle regulators cell cycle regulators

Schema {🗺️}

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         headline:Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice
         description:The constitutive inflammation that characterizes advanced age is termed inflamm-aging. This process is associated with age-related changes to immune homeostasis and gut microbiota. We investigated the relationship between aging and gut microbiota lipopolysaccharide (LPS)-inducible inflammation. A taxonomy-based analysis showed that aging resulted in increased prevalence of the phyla Firmicutes and Actinobacteria and a reduced prevalence of Bacteroidetes and Tenericutes, resulting in an increase in the Firmicutes to Bacteroidetes ratio. The levels of plasmatic and fecal lipopolysaccharides were higher in aged mice. Aging induced the expression of p16 and the activation of nuclear factor-kappa B (NF-κB) in the colon of aged mice. Interestingly, the expression level of sterile α-motif domain- and HD domain-containing protein 1 (SAMHD1) in the colon was higher in aged mice than in young mice, while cyclin-dependent kinase-2 and cyclin E levels were lower in aged mice than in young mice. The lipopolysaccharide fraction of fecal lysates (LFL) from young or aged mice increased p16 and SAMHD1 expression and NF-κB activation in peritoneal macrophages from wild-type mice, in a TLR4-dependent manner. However, LFLs did not induce NF-κB activation and SAMHD1 expression in peritoneal macrophages from TLR4-deificent mice, whereas they significantly induced p16 expression. Nevertheless, p16 expression was induced more potently in macrophages from WT mice than in macrophages from TLR4-deficient mice. Aging increased p16 and SAMHD1 expression, gut microbiota LPS production, and NF-κB activation; thereby, signifying that gut microbiota LPS may accelerate inflamm-aging and SAMHD1 may be an inflamm-aging marker.
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      headline:Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice
      description:The constitutive inflammation that characterizes advanced age is termed inflamm-aging. This process is associated with age-related changes to immune homeostasis and gut microbiota. We investigated the relationship between aging and gut microbiota lipopolysaccharide (LPS)-inducible inflammation. A taxonomy-based analysis showed that aging resulted in increased prevalence of the phyla Firmicutes and Actinobacteria and a reduced prevalence of Bacteroidetes and Tenericutes, resulting in an increase in the Firmicutes to Bacteroidetes ratio. The levels of plasmatic and fecal lipopolysaccharides were higher in aged mice. Aging induced the expression of p16 and the activation of nuclear factor-kappa B (NF-κB) in the colon of aged mice. Interestingly, the expression level of sterile α-motif domain- and HD domain-containing protein 1 (SAMHD1) in the colon was higher in aged mice than in young mice, while cyclin-dependent kinase-2 and cyclin E levels were lower in aged mice than in young mice. The lipopolysaccharide fraction of fecal lysates (LFL) from young or aged mice increased p16 and SAMHD1 expression and NF-κB activation in peritoneal macrophages from wild-type mice, in a TLR4-dependent manner. However, LFLs did not induce NF-κB activation and SAMHD1 expression in peritoneal macrophages from TLR4-deificent mice, whereas they significantly induced p16 expression. Nevertheless, p16 expression was induced more potently in macrophages from WT mice than in macrophages from TLR4-deficient mice. Aging increased p16 and SAMHD1 expression, gut microbiota LPS production, and NF-κB activation; thereby, signifying that gut microbiota LPS may accelerate inflamm-aging and SAMHD1 may be an inflamm-aging marker.
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         Parasitology
         Virology
         Life Sciences
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