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N-acetylcysteine modulates lipopolysaccharide-induced intestinal dysfunction
The gastrointestinal epithelium functions in nutrient absorption and pathogens barrier and its dysfunction directly affects livestock performance. N-Acetylcysteine (NAC) improves mucosal function, but its effects on intestinal functions at the molecular level remain unclear. Here, we performed gene...
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description | The gastrointestinal epithelium functions in nutrient absorption and pathogens barrier and its dysfunction directly affects livestock performance. N-Acetylcysteine (NAC) improves mucosal function, but its effects on intestinal functions at the molecular level remain unclear. Here, we performed gene expression profiling of the pig small intestine after dietary NAC treatment under LPS challenge and investigated the effects of NAC on intestinal epithelial cells
in vitro
. Dietary NAC supplementation under LPS challenge altered the small intestine expression of 959 genes related to immune response, inflammatory response, oxidation-reduction process, cytokine-cytokine receptor interaction, and the cytokine-mediated signalling, Toll-like receptor signalling pathway, Jak-STAT signalling pathway, and TNF signalling pathway. We then analysed the expression patterns of the top 10 altered genes, and found that NAC markedly stimulated
HMGCS3
and
LDHC
expression in IPEC-J2 cells.
In vitro
, NAC pre-treatment significantly reduced TNF-α and
NF-κB
,
TNF-α
,
IFN-γ
, and
IL-6
expression in LPS-induced IPEC-J2 cells. NAC treatment also significantly reduced oxidative stress in LPS-induced IPEC-J2 cells and alleviated intestinal barrier function and wound healing. Thus, NAC as a feed additive can enhance livestock intestinal health by modulating intestinal inflammation, permeability, and wound healing under LPS-induced dysfunction, improving our molecular understanding of the effects of NAC on the intestine. |
doi_str_mv | 10.1038/s41598-018-37296-x |
format | article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6353963</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2179476027</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-d5550af1c81f1d9017f5be5c62ac4e9e7b5916fa3b5c17d1820b2ec0b64c07bf3</originalsourceid><addsrcrecordid>eNp9kcFvFSEQxonR2Kb2H_BgXuLFC3WAZVkuJqap2uRFL3omLMy2NDx4wq7p_vdiX63Vg3NhkvnNN3z5CHnJ4IyBGN7Wjkk9UGADFYrrnt4-IcccOkm54Pzpo_6InNZ6A60k1x3Tz8mRAAUwwHBMtp-pdTiv0a11xpBws8t-iXbGuolhn_c5rtU6d21L8EhD8otDvwmpAXNINm78WqcluTnk9II8m2yseHr_npBvHy6-nn-i2y8fL8_fb6nrVDdTL6UEOzE3sIl5DUxNckTpem5dhxrVKDXrJytG6ZjybOAwcnQw9p0DNU7ihLw76O6XcYfeYZqLjWZfws6W1WQbzN-TFK7NVf5heiGF7kUTeHMvUPL3pTkxu1AdxmgT5qUazpTuVA9cNfT1P-hNXkozfkcJ1TMGQ6P4gXIl11pwevgMA_MrL3PIy7S8zF1e5rYtvXps42HldzoNEAegtlG6wvLn9n9kfwKotaO2</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2173761108</pqid></control><display><type>article</type><title>N-acetylcysteine modulates lipopolysaccharide-induced intestinal dysfunction</title><source>PubMed (Medline)</source><source>Publicly Available Content Database</source><source>Free Full-Text Journals in Chemistry</source><source>Springer Nature - nature.com Journals - Fully Open Access</source><creator>Lee, Sang In ; Kang, Kyung Soo</creator><creatorcontrib>Lee, Sang In ; Kang, Kyung Soo</creatorcontrib><description>The gastrointestinal epithelium functions in nutrient absorption and pathogens barrier and its dysfunction directly affects livestock performance. N-Acetylcysteine (NAC) improves mucosal function, but its effects on intestinal functions at the molecular level remain unclear. Here, we performed gene expression profiling of the pig small intestine after dietary NAC treatment under LPS challenge and investigated the effects of NAC on intestinal epithelial cells
in vitro
. Dietary NAC supplementation under LPS challenge altered the small intestine expression of 959 genes related to immune response, inflammatory response, oxidation-reduction process, cytokine-cytokine receptor interaction, and the cytokine-mediated signalling, Toll-like receptor signalling pathway, Jak-STAT signalling pathway, and TNF signalling pathway. We then analysed the expression patterns of the top 10 altered genes, and found that NAC markedly stimulated
HMGCS3
and
LDHC
expression in IPEC-J2 cells.
In vitro
, NAC pre-treatment significantly reduced TNF-α and
NF-κB
,
TNF-α
,
IFN-γ
, and
IL-6
expression in LPS-induced IPEC-J2 cells. NAC treatment also significantly reduced oxidative stress in LPS-induced IPEC-J2 cells and alleviated intestinal barrier function and wound healing. Thus, NAC as a feed additive can enhance livestock intestinal health by modulating intestinal inflammation, permeability, and wound healing under LPS-induced dysfunction, improving our molecular understanding of the effects of NAC on the intestine.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-37296-x</identifier><identifier>PMID: 30700808</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>38/39 ; 38/77 ; 38/91 ; 631/601/1737 ; 631/61/191/2018 ; Acetylcysteine ; Acetylcysteine - pharmacology ; Animals ; Biomarkers - metabolism ; Cell Line ; Cytokines ; Dietary Supplements ; Enteritis - immunology ; Enteritis - metabolism ; Epithelial cells ; Epithelial Cells - cytology ; Epithelial Cells - metabolism ; Epithelium ; Feed additives ; Gene expression ; Humanities and Social Sciences ; Immune response ; Inflammation ; Interleukin 6 ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Intestine, Small - metabolism ; Intestine, Small - pathology ; Lipopolysaccharides ; Livestock ; Mucosa ; multidisciplinary ; NF-κB protein ; Oxidation-reduction potential ; Oxidative stress ; Permeability ; Science ; Science (multidisciplinary) ; Signal transduction ; Small intestine ; Swine - metabolism ; Swine, Miniature - metabolism ; Toll-like receptors ; Tumor necrosis factor-α ; Wound healing ; γ-Interferon</subject><ispartof>Scientific reports, 2019-01, Vol.9 (1), p.1004-1004, Article 1004</ispartof><rights>The Author(s) 2019</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-d5550af1c81f1d9017f5be5c62ac4e9e7b5916fa3b5c17d1820b2ec0b64c07bf3</citedby><cites>FETCH-LOGICAL-c474t-d5550af1c81f1d9017f5be5c62ac4e9e7b5916fa3b5c17d1820b2ec0b64c07bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2173761108/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2173761108?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768,74869</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30700808$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Sang In</creatorcontrib><creatorcontrib>Kang, Kyung Soo</creatorcontrib><title>N-acetylcysteine modulates lipopolysaccharide-induced intestinal dysfunction</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The gastrointestinal epithelium functions in nutrient absorption and pathogens barrier and its dysfunction directly affects livestock performance. N-Acetylcysteine (NAC) improves mucosal function, but its effects on intestinal functions at the molecular level remain unclear. Here, we performed gene expression profiling of the pig small intestine after dietary NAC treatment under LPS challenge and investigated the effects of NAC on intestinal epithelial cells
in vitro
. Dietary NAC supplementation under LPS challenge altered the small intestine expression of 959 genes related to immune response, inflammatory response, oxidation-reduction process, cytokine-cytokine receptor interaction, and the cytokine-mediated signalling, Toll-like receptor signalling pathway, Jak-STAT signalling pathway, and TNF signalling pathway. We then analysed the expression patterns of the top 10 altered genes, and found that NAC markedly stimulated
HMGCS3
and
LDHC
expression in IPEC-J2 cells.
In vitro
, NAC pre-treatment significantly reduced TNF-α and
NF-κB
,
TNF-α
,
IFN-γ
, and
IL-6
expression in LPS-induced IPEC-J2 cells. NAC treatment also significantly reduced oxidative stress in LPS-induced IPEC-J2 cells and alleviated intestinal barrier function and wound healing. Thus, NAC as a feed additive can enhance livestock intestinal health by modulating intestinal inflammation, permeability, and wound healing under LPS-induced dysfunction, improving our molecular understanding of the effects of NAC on the intestine.</description><subject>38/39</subject><subject>38/77</subject><subject>38/91</subject><subject>631/601/1737</subject><subject>631/61/191/2018</subject><subject>Acetylcysteine</subject><subject>Acetylcysteine - pharmacology</subject><subject>Animals</subject><subject>Biomarkers - metabolism</subject><subject>Cell Line</subject><subject>Cytokines</subject><subject>Dietary Supplements</subject><subject>Enteritis - immunology</subject><subject>Enteritis - metabolism</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelium</subject><subject>Feed additives</subject><subject>Gene expression</subject><subject>Humanities and Social Sciences</subject><subject>Immune response</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - pathology</subject><subject>Intestine, Small - metabolism</subject><subject>Intestine, Small - pathology</subject><subject>Lipopolysaccharides</subject><subject>Livestock</subject><subject>Mucosa</subject><subject>multidisciplinary</subject><subject>NF-κB protein</subject><subject>Oxidation-reduction potential</subject><subject>Oxidative stress</subject><subject>Permeability</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signal transduction</subject><subject>Small intestine</subject><subject>Swine - metabolism</subject><subject>Swine, Miniature - metabolism</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor-α</subject><subject>Wound healing</subject><subject>γ-Interferon</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNp9kcFvFSEQxonR2Kb2H_BgXuLFC3WAZVkuJqap2uRFL3omLMy2NDx4wq7p_vdiX63Vg3NhkvnNN3z5CHnJ4IyBGN7Wjkk9UGADFYrrnt4-IcccOkm54Pzpo_6InNZ6A60k1x3Tz8mRAAUwwHBMtp-pdTiv0a11xpBws8t-iXbGuolhn_c5rtU6d21L8EhD8otDvwmpAXNINm78WqcluTnk9II8m2yseHr_npBvHy6-nn-i2y8fL8_fb6nrVDdTL6UEOzE3sIl5DUxNckTpem5dhxrVKDXrJytG6ZjybOAwcnQw9p0DNU7ihLw76O6XcYfeYZqLjWZfws6W1WQbzN-TFK7NVf5heiGF7kUTeHMvUPL3pTkxu1AdxmgT5qUazpTuVA9cNfT1P-hNXkozfkcJ1TMGQ6P4gXIl11pwevgMA_MrL3PIy7S8zF1e5rYtvXps42HldzoNEAegtlG6wvLn9n9kfwKotaO2</recordid><startdate>20190130</startdate><enddate>20190130</enddate><creator>Lee, Sang In</creator><creator>Kang, Kyung Soo</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190130</creationdate><title>N-acetylcysteine modulates lipopolysaccharide-induced intestinal dysfunction</title><author>Lee, Sang In ; Kang, Kyung Soo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-d5550af1c81f1d9017f5be5c62ac4e9e7b5916fa3b5c17d1820b2ec0b64c07bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>38/39</topic><topic>38/77</topic><topic>38/91</topic><topic>631/601/1737</topic><topic>631/61/191/2018</topic><topic>Acetylcysteine</topic><topic>Acetylcysteine - pharmacology</topic><topic>Animals</topic><topic>Biomarkers - metabolism</topic><topic>Cell Line</topic><topic>Cytokines</topic><topic>Dietary Supplements</topic><topic>Enteritis - immunology</topic><topic>Enteritis - metabolism</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelium</topic><topic>Feed additives</topic><topic>Gene expression</topic><topic>Humanities and Social Sciences</topic><topic>Immune response</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestine, Small - metabolism</topic><topic>Intestine, Small - pathology</topic><topic>Lipopolysaccharides</topic><topic>Livestock</topic><topic>Mucosa</topic><topic>multidisciplinary</topic><topic>NF-κB protein</topic><topic>Oxidation-reduction potential</topic><topic>Oxidative stress</topic><topic>Permeability</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Signal transduction</topic><topic>Small intestine</topic><topic>Swine - metabolism</topic><topic>Swine, Miniature - metabolism</topic><topic>Toll-like receptors</topic><topic>Tumor necrosis factor-α</topic><topic>Wound healing</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Sang In</creatorcontrib><creatorcontrib>Kang, Kyung Soo</creatorcontrib><collection>SpringerOpen</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Sang In</au><au>Kang, Kyung Soo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>N-acetylcysteine modulates lipopolysaccharide-induced intestinal dysfunction</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-01-30</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>1004</spage><epage>1004</epage><pages>1004-1004</pages><artnum>1004</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The gastrointestinal epithelium functions in nutrient absorption and pathogens barrier and its dysfunction directly affects livestock performance. N-Acetylcysteine (NAC) improves mucosal function, but its effects on intestinal functions at the molecular level remain unclear. Here, we performed gene expression profiling of the pig small intestine after dietary NAC treatment under LPS challenge and investigated the effects of NAC on intestinal epithelial cells
in vitro
. Dietary NAC supplementation under LPS challenge altered the small intestine expression of 959 genes related to immune response, inflammatory response, oxidation-reduction process, cytokine-cytokine receptor interaction, and the cytokine-mediated signalling, Toll-like receptor signalling pathway, Jak-STAT signalling pathway, and TNF signalling pathway. We then analysed the expression patterns of the top 10 altered genes, and found that NAC markedly stimulated
HMGCS3
and
LDHC
expression in IPEC-J2 cells.
In vitro
, NAC pre-treatment significantly reduced TNF-α and
NF-κB
,
TNF-α
,
IFN-γ
, and
IL-6
expression in LPS-induced IPEC-J2 cells. NAC treatment also significantly reduced oxidative stress in LPS-induced IPEC-J2 cells and alleviated intestinal barrier function and wound healing. Thus, NAC as a feed additive can enhance livestock intestinal health by modulating intestinal inflammation, permeability, and wound healing under LPS-induced dysfunction, improving our molecular understanding of the effects of NAC on the intestine.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30700808</pmid><doi>10.1038/s41598-018-37296-x</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 38/39 38/77 38/91 631/601/1737 631/61/191/2018 Acetylcysteine Acetylcysteine - pharmacology Animals Biomarkers - metabolism Cell Line Cytokines Dietary Supplements Enteritis - immunology Enteritis - metabolism Epithelial cells Epithelial Cells - cytology Epithelial Cells - metabolism Epithelium Feed additives Gene expression Humanities and Social Sciences Immune response Inflammation Interleukin 6 Intestinal Mucosa - metabolism Intestinal Mucosa - pathology Intestine, Small - metabolism Intestine, Small - pathology Lipopolysaccharides Livestock Mucosa multidisciplinary NF-κB protein Oxidation-reduction potential Oxidative stress Permeability Science Science (multidisciplinary) Signal transduction Small intestine Swine - metabolism Swine, Miniature - metabolism Toll-like receptors Tumor necrosis factor-α Wound healing γ-Interferon |
title | N-acetylcysteine modulates lipopolysaccharide-induced intestinal dysfunction |
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