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Agarooligosaccharides as a novel concept in prebiotics: selective inhibition of and while preserving Bifidobacteria, Lactobacillales , and inhibiting Lachnospiraceae . | LitMetric

AI Article Synopsis

  • * AOS treatment alters fatty acid composition in bacterial cell membranes, increasing medium-chain and C18 fatty acids while decreasing long-chain fatty acids, indicating a change in bacterial metabolism.
  • * Studies in mice show AOS administration leads to a reduction in specific bacteria linked to inflammation, highlighting potential benefits in managing inflammatory bowel disease and promoting gut health.

Article Abstract

Recent studies have linked to inflammatory bowel disease and to various cancers. Agarooligosaccharides (AOS), derived from the acid hydrolysis of agar, have shown significant inhibitory effects on the growth of and at concentrations of 0.1 and 0.2%, respectively. RNA sequencing and quantitative reverse-transcription PCR analyses revealed the downregulation of fatty acid biosynthesis genes ( genes) in these bacteria when exposed to 0.1% AOS. Furthermore, AOS treatment altered the fatty acid composition of cell membranes, increasing medium-chain saturated fatty acids (C8, C10) and C18 fatty acids while reducing long-chain fatty acids (C14, C16). In contrast, no significant growth inhibition was observed in several strains of Bifidobacteria and Lactobacillales at AOS concentrations of 0.2 and 2%, respectively. Co-culture experiments with and in 0.2% AOS resulted in dominating the population, constituting over 96% post-incubation. studies using mice demonstrated a significant reduction in the Lachnospiraceae family, to which belongs, following AOS administration. Quantitative PCR also showed lower levels of the gene, potentially associated with immune disorders, in the AOS group. These findings suggest that AOS may introduce a novel concept in prebiotics by selectively inhibiting potentially pathogenic bacteria while preserving beneficial bacteria such as Bifidobacteria and Lactobacillales.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581127PMC
http://dx.doi.org/10.1099/mic.0.001510DOI Listing

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