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• W1945764404 abstract "Background: The integrity of the epithelial layer in the gastrointestinal tract protects organisms from exposure to luminal antigens, which are considered the primary cause of chronic intestinal inflammation and allergic responses. The common wheat-associated fungal toxin deoxynivalenol acts as a specific disruptor of the intestinal tight junction network and hence might contribute to the pathogenesis of inflammatory bowel diseases. Objective: The aim of the current study was to assess whether defined galacto-oligosaccharides (GOSs) can prevent deoxynivalenol-induced epithelial dysfunction. Methods: Human epithelial intestinal Caco-2 cells, pretreated with different concentrations of GOSs (0.5%, 1%, and 2%) for 24 h, were stimulated with 4.2-μM deoxynivalenol (24 h), and 6/7-wk-old male B6C3F1 mice were fed a diet supplemented with 1% GOSs for 2 wk before being orally exposed to deoxynivalenol (25 mg/kg body weight, 6 h). Barrier integrity was determined by measuring transepithelial electrical resistance (TEER) and intestinal permeability to marker molecules. A calcium switch assay was conducted to study the assembly of epithelial tight junction proteins. Alterations in tight junction and cytokine expression were assessed by quantitative reverse transcriptase-polymerase chain reaction, Western blot analysis, or ELISA, and their localization was visualized by immunofluorescence microscopy. Sections of the proximal and distal small intestine were stained with hematoxylin/eosin for histomorphometric analysis. Results: The in vitro data showed that medium supplemented with 2% GOSs improved tight junction assembly reaching an acceleration of 85% after 6 h (P < 0.05). In turn, GOSs prevented the deoxynivalenol-induced loss of epithelial barrier function as measured by TEER (114% of control), and paracellular flux of Lucifer yellow (82.7% of prechallenge values, P < 0.05). Moreover, GOSs stabilized the expression and cellular distribution of claudin3 and suppressed by >50% the deoxynivalenol-induced synthesis and release of interleukin-8 [IL8/chemokine CXC motif ligand (CXCL8)] (P < 0.05). In mice, GOSs prevented the deoxynivalenol-induced mRNA overexpression of claudin3 (P = 0.022) and CXCL8 homolog keratinocyte hemoattractant (Kc) (Cxcl1) (P = 0.06) as well as the deoxynivalenol-induced morphologic defects. Conclusions: The results demonstrate that GOSs stimulate the tight junction assembly and in turn mitigate the deleterious effects of deoxynivalenol on the intestinal barrier of Caco-2 cells and on villus architecture of B6C3F1 mice." @default.
• W1945764404 created "2016-06-24" @default.
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• W1945764404 date "2015-07-01" @default.
• W1945764404 modified "2023-10-16" @default.
• W1945764404 title "Galacto-oligosaccharides Protect the Intestinal Barrier by Maintaining the Tight Junction Network and Modulating the Inflammatory Responses after a Challenge with the Mycotoxin Deoxynivalenol in Human Caco-2 Cell Monolayers and B6C3F1 Mice" @default.
• W1945764404 cites W1523737655 @default.
• W1945764404 cites W1831301545 @default.
• W1945764404 cites W1832400618 @default.
• W1945764404 cites W1943641126 @default.
• W1945764404 cites W1964339238 @default.
• W1945764404 cites W1969954634 @default.
• W1945764404 cites W1970859421 @default.
• W1945764404 cites W1974477809 @default.
• W1945764404 cites W1974598127 @default.
• W1945764404 cites W1976800458 @default.
• W1945764404 cites W1982914684 @default.
• W1945764404 cites W1987265868 @default.
• W1945764404 cites W1992152055 @default.
• W1945764404 cites W1993984872 @default.
• W1945764404 cites W1994939538 @default.
• W1945764404 cites W1997952530 @default.
• W1945764404 cites W1999283861 @default.
• W1945764404 cites W2000422049 @default.
• W1945764404 cites W2001721904 @default.
• W1945764404 cites W2001944304 @default.
• W1945764404 cites W2003053114 @default.
• W1945764404 cites W2005303890 @default.
• W1945764404 cites W2010901488 @default.
• W1945764404 cites W2012530210 @default.
• W1945764404 cites W2012818587 @default.
• W1945764404 cites W2015734501 @default.
• W1945764404 cites W2027510691 @default.
• W1945764404 cites W2031624408 @default.
• W1945764404 cites W2032612084 @default.
• W1945764404 cites W2033247222 @default.
• W1945764404 cites W2034939204 @default.
• W1945764404 cites W2035390600 @default.
• W1945764404 cites W2035475717 @default.
• W1945764404 cites W2036483246 @default.
• W1945764404 cites W2038269648 @default.
• W1945764404 cites W2045545069 @default.
• W1945764404 cites W2047285075 @default.
• W1945764404 cites W2050226660 @default.
• W1945764404 cites W2054371494 @default.
• W1945764404 cites W2055651239 @default.
• W1945764404 cites W2057086723 @default.
• W1945764404 cites W2066063288 @default.
• W1945764404 cites W2068634673 @default.
• W1945764404 cites W2086006111 @default.
• W1945764404 cites W2088810826 @default.
• W1945764404 cites W2095655966 @default.
• W1945764404 cites W2098518081 @default.
• W1945764404 cites W2101656923 @default.
• W1945764404 cites W2108635800 @default.
• W1945764404 cites W2112821425 @default.
• W1945764404 cites W2120950548 @default.
• W1945764404 cites W2120962670 @default.
• W1945764404 cites W2124226554 @default.
• W1945764404 cites W2126490333 @default.
• W1945764404 cites W2130952545 @default.
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• W1945764404 cites W2149199388 @default.
• W1945764404 cites W2149899704 @default.
• W1945764404 cites W2152751713 @default.
• W1945764404 cites W2154612703 @default.
• W1945764404 cites W2165754609 @default.
• W1945764404 cites W2168118833 @default.
• W1945764404 cites W2419192646 @default.
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• W1945764404 doi "https://doi.org/10.3945/jn.114.209486" @default.
• W1945764404 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26019243" @default.
• W1945764404 hasPublicationYear "2015" @default.
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