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• W3097806051 abstract "Background and Aims: Following a fat-rich diet, alterations in gut microbiota contribute to enhanced gut permeability, metabolic endotoxemia, and low grade inflammation–associated metabolic disorders. To better understand whether commensal bifidobacteria influence the expression of key metaflammation-related biomarkers (chemerin, MCP-1, PEDF) and modulate the pro-inflammatory bacteria- and lipid–coupled intracellular signaling pathways, we aimed at i) investigating the influence of the establishment of microbial signaling molecules-based cell-cell contacts on the involved intercellular communication between enterocytes, immune cells, and adipocytes, and ii) assessing their inflammatory mediators’ expression profiles within an inflamed adipose tissue model. Material and Methods: Bifidobacterium animalis R101-8 and Escherichia coli TG1, respectively, were added to the apical side of a triple co-culture model consisting of intestinal epithelial HT-29/B6 cell line, human monocyte-derived macrophage cells, and adipose-derived stem cell line in the absence or presence of LPS or palmitic acid. mRNA expression levels of key lipid metabolism genes HILPDA, MCP-1/CCL2, RARRES2, SCD, SFRP2 and TLR4 were determined using TaqMan qRT-PCR. Protein expression levels of cytokines (IL-1β, IL-6, and TNF-α), key metaflammation-related biomarkers including adipokines (chemerin and PEDF), chemokine (MCP- 1) as well as cellular triglycerides were assessed by cell-based ELISA, while those of p-ERK, p-JNK, p-p38, NF-κB, p-IκBα, pc-Fos, pc-Jun, and TLR4 were assessed by Western blotting. Results: B. animalis R101-8 inhibited LPS- and palmitic acid-induced protein expression of inflammatory cytokines IL-1β, IL-6, TNF-α concomitant with decreases in chemerin, MCP-1, PEDF, and cellular triglycerides, and blocked NF-kB and AP-1 activation pathway through inhibition of p- IκBα, pc-Jun, and pc-Fos phosphorylation. B. animalis R101-8 downregulated mRNA and protein levels of HILPDA, MCP-1/CCL2, RARRES2, SCD and SFRP2 and TLR4 following exposure to LPS and palmitic acid. Conclusion: B. animalis R101-8 improves biomarkers of metaflammation through at least two molecular/signaling mechanisms 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 the 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." @default.
• W3097806051 created "2020-11-09" @default.
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• W3097806051 date "2021-06-01" @default.
• W3097806051 modified "2023-09-27" @default.
• W3097806051 title "Modulation of Proinflammatory Bacteria- and Lipid-Coupled Intracellular Signaling Pathways in a Transwell Triple Co-Culture Model by Commensal Bifidobacterium Animalis R101-8" @default.
• W3097806051 cites W1793370695 @default.
• W3097806051 cites W1969681272 @default.
• W3097806051 cites W1974509866 @default.
• W3097806051 cites W1984238073 @default.
• W3097806051 cites W1985744009 @default.
• W3097806051 cites W1986753065 @default.
• W3097806051 cites W1996018346 @default.
• W3097806051 cites W1999643046 @default.
• W3097806051 cites W1999816171 @default.
• W3097806051 cites W2021951862 @default.
• W3097806051 cites W2022577922 @default.
• W3097806051 cites W2025867886 @default.
• W3097806051 cites W2027131478 @default.
• W3097806051 cites W2030601829 @default.
• W3097806051 cites W2066968550 @default.
• W3097806051 cites W2070127118 @default.
• W3097806051 cites W2083979121 @default.
• W3097806051 cites W2091400895 @default.
• W3097806051 cites W2092044051 @default.
• W3097806051 cites W2100399616 @default.
• W3097806051 cites W2110103499 @default.
• W3097806051 cites W2115742500 @default.
• W3097806051 cites W2118143118 @default.
• W3097806051 cites W2130220323 @default.
• W3097806051 cites W2144801651 @default.
• W3097806051 cites W2148090028 @default.
• W3097806051 cites W2399428158 @default.
• W3097806051 cites W2407256458 @default.
• W3097806051 cites W244067736 @default.
• W3097806051 cites W2461706302 @default.
• W3097806051 cites W2464484550 @default.
• W3097806051 cites W2473078753 @default.
• W3097806051 cites W2572439880 @default.
• W3097806051 cites W2587680743 @default.
• W3097806051 cites W2594242670 @default.
• W3097806051 cites W2742247528 @default.
• W3097806051 cites W2743628312 @default.
• W3097806051 cites W2754174764 @default.
• W3097806051 cites W2767614677 @default.
• W3097806051 cites W2774237522 @default.
• W3097806051 cites W2774458980 @default.
• W3097806051 cites W2794942947 @default.
• W3097806051 cites W2803286167 @default.
• W3097806051 cites W2809948365 @default.
• W3097806051 cites W2892527163 @default.
• W3097806051 cites W2895612816 @default.
• W3097806051 cites W2896000850 @default.
• W3097806051 cites W2898312618 @default.
• W3097806051 cites W2906764434 @default.
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• W3097806051 doi "https://doi.org/10.2174/1871523019999201029115618" @default.
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