Bacteroides cellulosilyticus and Bacteroides xylanisolvens may have anti-inflammatory and strain-specific neuromodulatory effects.
Evidence
This in vitro and animal-model study tested two human gut Bacteroides isolates in Caco-2 cells, Caco-2/PBMC cocultures, and Caenorhabditis elegans.
Caveat
Cell and worm gene-expression models do not establish effects on human gut-brain signaling or neuropsychiatric outcomes.
Simplified
Alterations in the abundance of Bacteroides species are linked to the disruption of the intestinal epithelial barrier and chronic inflammation and has been increasingly recognized as a factor in the development of neurological and neuropsychiatric disorders. Nevertheless, the exact role of Bacteroides species in the gut-brain cross-talk is still largely unexplored. Here, we investigated the immunoregulatory and neuromodulatory potential of two poorly characterized Bacteroides species, including Bacteroides cellulosilyticus and Bacteroides xylanisolvens. The results revealed that both Bacteroides isolates reduced inflammation in Caco-2 intestinal epithelial cells by decreasing the level of IL-8 chemokine and transcription of NF-kB, the two key factors involved in gut inflammation development and barrier disruption. In addition, the Bacteroides strains in the co-culture of Caco-2 cells and phytohemagglutinin-stimulated PBMCs reduced the production of pro-inflammatory cytokines TNF-α and IL-1β, as well as Th1-polarizing IFN-γ cytokine. Finally, in Caenorhabditis elegans, Bacteroides strains differently modulated the expression of the genes implicated in GABA, serotonin and dopamine signaling and synaptic vesicles release pointed to the strain-specific effects of these isolates on neural function. Altogether, these in vitro results show that tested Bacteroides strains may exert anti-inflammatory and neuromodulatory effects, indicating their potential role in microbiota-.
Key numbers
17×
Decrease in Levels
Reduction in levels in after treatment with strains.
2 of 4
Decrease in TNF-α Production
Reduction in TNF-α production in co-cultured with treated with .
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