Modulation of proinflammatory bacteria- and lipid-coupled intracellular signaling pathways in a transwell triple co-culture model by commensal Bifidobacterium animalis R101-8.

B. animalis R101-8 improves biomarkers of metaflammation through at least two molecular/signaling mechanisms that are triggered by pro-inflammatory bacteria/lipids. First, B. animalis R101-8 modulates the coupled intracellular signaling pathways via metabolizing saturated fatty acids and reducing available bioactive palmitic acid. Second, it inhibits NF-kB's and AP-1's transcriptional activities, resulting in reduction of pro-inflammatory markers. Thus, the molecular basis may be formed by which commensal bifidobacteria improve intrinsic cellular tolerance against excess pro-inflammatory lipids, and participate in homeostatic regulation of metabolic processes in vivo.