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• W4224881353 endingPage "110738" @default.
• W4224881353 startingPage "110738" @default.
• W4224881353 abstract "Perturbed gut microbiome development has been linked to childhood malnutrition. Here, we characterize bacterial Toll/interleukin-1 receptor (TIR) protein domains that metabolize nicotinamide adenine dinucleotide (NAD), a co-enzyme with far-reaching effects on human physiology. A consortium of 26 human gut bacterial strains, representing the diversity of TIRs observed in the microbiome and the NAD hydrolase (NADase) activities of a subset of 152 bacterial TIRs assayed in vitro, was introduced into germ-free mice. Integrating mass spectrometry and microbial RNA sequencing (RNA-seq) with consortium membership manipulation disclosed that a variant of cyclic-ADPR (v-cADPR-x) is a specific product of TIR NADase activity and a prominent, colonization-discriminatory, taxon-specific metabolite. Guided by bioinformatic analyses of biochemically validated TIRs, we find that acute malnutrition is associated with decreased fecal levels of genes encoding TIRs known or predicted to generate v-cADPR-x, as well as decreased levels of the metabolite itself. These results underscore the need to consider microbiome TIR NADases when evaluating NAD metabolism in the human holobiont." @default.
• W4224881353 created "2022-04-27" @default.
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• W4224881353 date "2022-04-01" @default.
• W4224881353 modified "2023-10-14" @default.
• W4224881353 title "Products of gut microbial Toll/interleukin-1 receptor domain NADase activities in gnotobiotic mice and Bangladeshi children with malnutrition" @default.
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• W4224881353 doi "https://doi.org/10.1016/j.celrep.2022.110738" @default.
• W4224881353 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35476981" @default.
• W4224881353 hasPublicationYear "2022" @default.
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