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• W1989874363 endingPage "46" @default.
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• W1989874363 abstract "<h3>Background</h3> A major cause of enteric infection, Gram-negative pathogenic bacteria activate mucosal inflammation through lipopolysaccharide (LPS) binding to intestinal toll-like receptor 4 (TLR4). Breast feeding lowers risk of disease, and human milk modulates inflammation. <h3>Objective</h3> This study tested whether human milk oligosaccharides (HMOSs) influence pathogenic <i>Escherichia coli</i>-induced interleukin (IL)-8 release by intestinal epithelial cells (IECs), identified specific proinflammatory signalling molecules modulated by HMOSs, specified the active HMOS and determined its mechanism of action. <h3>Methods</h3> Models of inflammation were IECs invaded by type 1 pili enterotoxigenic <i>E. coli</i> (ETEC) in vitro: T84 modelled mature, and H4 modelled immature IECs. LPS-induced signalling molecules co-varying with IL-8 release in the presence or absence of HMOSs were identified. Knockdown and overexpression verified signalling mediators. The oligosaccharide responsible for altered signalling was identified. <h3>Results</h3> HMOSs attenuated LPS-dependent induction of IL-8 caused by ETEC, uropathogenic <i>E. coli</i>, and adherent-invasive <i>E. coli</i> (AIEC) infection, and suppressed CD14 transcription and translation. CD14 knockdown recapitulated HMOS-induced attenuation. Overexpression of CD14 increased the inflammatory response to ETEC and sensitivity to inhibition by HMOSs. 2′-fucosyllactose (2′-FL), at milk concentrations, displayed equivalent ability as total HMOSs to suppress CD14 expression, and protected AIEC-infected mice. <h3>Conclusions</h3> HMOSs and 2′-FL directly inhibit LPS-mediated inflammation during ETEC invasion of T84 and H4 IECs through attenuation of CD14 induction. CD14 expression mediates LPS-TLR4 stimulation of portions of the ‘macrophage migration inhibitory factors’ inflammatory pathway via suppressors of cytokine signalling 2/signal transducer and activator of transcription 3/NF-κB. HMOS direct inhibition of inflammation supports its functioning as an innate immune system whereby the mother protects her vulnerable neonate through her milk. 2′-FL, a principal HMOS, quenches inflammatory signalling." @default.
• W1989874363 created "2016-06-24" @default.
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• W1989874363 date "2014-11-27" @default.
• W1989874363 modified "2023-10-01" @default.
• W1989874363 title "The human milk oligosaccharide 2′-fucosyllactose modulates CD14 expression in human enterocytes, thereby attenuating LPS-induced inflammation" @default.
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• W1989874363 doi "https://doi.org/10.1136/gutjnl-2014-307544" @default.
• W1989874363 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25431457" @default.

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