Markers of activated inflammatory cells are associated with disease severity and intestinal microbiota in adults with non‑alcoholic fatty liver disease
Several mechanisms contribute to the pathogenesis of non‑alcoholic fatty liver disease (NAFLD). The intestinal microbiota (IM) and liver immune cells (LIC) may serve a role, but there has been no previous study assessing potential associations between IM and LIC. The aim of the present study was to...
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Veröffentlicht in: | International journal of molecular medicine 2018-10, Vol.42 (4), p.2229-2237 |
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description | Several mechanisms contribute to the pathogenesis of non‑alcoholic fatty liver disease (NAFLD). The intestinal microbiota (IM) and liver immune cells (LIC) may serve a role, but there has been no previous study assessing potential associations between IM and LIC. The aim of the present study was to investigate whether there are differences in LIC markers between patients with NAFLD and healthy controls (HC), and to determine whether these markers are associated with specific IM. The present prospective, cross‑sectional study examined a cohort of adults with liver biopsy‑confirmed NAFLD and HC. Clinical and laboratory data were collected. Fecal IM was assessed by quantitative polymerase chain reaction and LIC, by immunohistochemistry. NAFLD activity score (NAS) was used for disease severity. Liver immune cell counts were increased in patients with NAFLD (n=34) vs. HC (n=8) and this was associated with disease severity. Hematopoietic cell marker cluster of differentiation (CD)45+ and Kupffer cell marker CD163+ were higher in NAFLD compared with HC, and those with an NAS ≥5 had higher levels of CD20+ cells, a marker of B cells, vs. a NAS of 0 or 1‑4. Additionally, from those patients (5 HC, 34 NAFLD), IM was measured. Specific immune cells in portal or lobular areas correlated with specific fecal IM, suggesting a potential association between IM and liver inflammation in patients with NAFLD. Specifically, Faecalibacterium prausnitzii was negatively correlated with CD45+ (r= ‑0.394; P=0.015) and CD163+ (r= ‑0.371; P=0.022) cells in the portal tract and Prevotella was negatively correlated with CD20+ (r= ‑0.353; P=0.028) cells in the liver lobule. Other taxa exhibited no correlation. In conclusion, the present study demonstrated a potential association between IM and liver inflammation in NAFLD. |
doi_str_mv | 10.3892/ijmm.2018.3800 |
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The intestinal microbiota (IM) and liver immune cells (LIC) may serve a role, but there has been no previous study assessing potential associations between IM and LIC. The aim of the present study was to investigate whether there are differences in LIC markers between patients with NAFLD and healthy controls (HC), and to determine whether these markers are associated with specific IM. The present prospective, cross‑sectional study examined a cohort of adults with liver biopsy‑confirmed NAFLD and HC. Clinical and laboratory data were collected. Fecal IM was assessed by quantitative polymerase chain reaction and LIC, by immunohistochemistry. NAFLD activity score (NAS) was used for disease severity. Liver immune cell counts were increased in patients with NAFLD (n=34) vs. HC (n=8) and this was associated with disease severity. Hematopoietic cell marker cluster of differentiation (CD)45+ and Kupffer cell marker CD163+ were higher in NAFLD compared with HC, and those with an NAS ≥5 had higher levels of CD20+ cells, a marker of B cells, vs. a NAS of 0 or 1‑4. Additionally, from those patients (5 HC, 34 NAFLD), IM was measured. Specific immune cells in portal or lobular areas correlated with specific fecal IM, suggesting a potential association between IM and liver inflammation in patients with NAFLD. Specifically, Faecalibacterium prausnitzii was negatively correlated with CD45+ (r= ‑0.394; P=0.015) and CD163+ (r= ‑0.371; P=0.022) cells in the portal tract and Prevotella was negatively correlated with CD20+ (r= ‑0.353; P=0.028) cells in the liver lobule. Other taxa exhibited no correlation. In conclusion, the present study demonstrated a potential association between IM and liver inflammation in NAFLD.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2018.3800</identifier><identifier>PMID: 30085339</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Alcohol ; Architects ; Automation ; Biopsy ; Care and treatment ; Cytokines ; Development and progression ; Fasting ; Fatty liver ; Genetic aspects ; Glucose ; Health aspects ; Histology ; Host-bacteria relationships ; Immunologic factors ; Inflammation ; Insulin resistance ; Laboratories ; Liver diseases ; Microbiota ; Microbiota (Symbiotic organisms) ; Pediatrics ; Rodents ; Studies</subject><ispartof>International journal of molecular medicine, 2018-10, Vol.42 (4), p.2229-2237</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-98a2d940709e1b4d2c6ee45ba087bf3edd5da3c7db2ec5bdd641b483f2c566263</citedby><cites>FETCH-LOGICAL-c391t-98a2d940709e1b4d2c6ee45ba087bf3edd5da3c7db2ec5bdd641b483f2c566263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30085339$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schwenger, Katherine J P</creatorcontrib><creatorcontrib>Chen, Lina</creatorcontrib><creatorcontrib>Chelliah, Adeline</creatorcontrib><creatorcontrib>Da Silva, Hannah E</creatorcontrib><creatorcontrib>Teterina, Anastasia</creatorcontrib><creatorcontrib>Comelli, Elena M</creatorcontrib><creatorcontrib>Taibi, Amel</creatorcontrib><creatorcontrib>Arendt, Bianca M</creatorcontrib><creatorcontrib>Fischer, Sandra</creatorcontrib><creatorcontrib>Allard, Johane P</creatorcontrib><title>Markers of activated inflammatory cells are associated with disease severity and intestinal microbiota in adults with non‑alcoholic fatty liver disease</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Several mechanisms contribute to the pathogenesis of non‑alcoholic fatty liver disease (NAFLD). The intestinal microbiota (IM) and liver immune cells (LIC) may serve a role, but there has been no previous study assessing potential associations between IM and LIC. The aim of the present study was to investigate whether there are differences in LIC markers between patients with NAFLD and healthy controls (HC), and to determine whether these markers are associated with specific IM. The present prospective, cross‑sectional study examined a cohort of adults with liver biopsy‑confirmed NAFLD and HC. Clinical and laboratory data were collected. Fecal IM was assessed by quantitative polymerase chain reaction and LIC, by immunohistochemistry. NAFLD activity score (NAS) was used for disease severity. Liver immune cell counts were increased in patients with NAFLD (n=34) vs. HC (n=8) and this was associated with disease severity. Hematopoietic cell marker cluster of differentiation (CD)45+ and Kupffer cell marker CD163+ were higher in NAFLD compared with HC, and those with an NAS ≥5 had higher levels of CD20+ cells, a marker of B cells, vs. a NAS of 0 or 1‑4. Additionally, from those patients (5 HC, 34 NAFLD), IM was measured. Specific immune cells in portal or lobular areas correlated with specific fecal IM, suggesting a potential association between IM and liver inflammation in patients with NAFLD. Specifically, Faecalibacterium prausnitzii was negatively correlated with CD45+ (r= ‑0.394; P=0.015) and CD163+ (r= ‑0.371; P=0.022) cells in the portal tract and Prevotella was negatively correlated with CD20+ (r= ‑0.353; P=0.028) cells in the liver lobule. Other taxa exhibited no correlation. In conclusion, the present study demonstrated a potential association between IM and liver inflammation in NAFLD.</description><subject>Alcohol</subject><subject>Architects</subject><subject>Automation</subject><subject>Biopsy</subject><subject>Care and treatment</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Fasting</subject><subject>Fatty liver</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Health aspects</subject><subject>Histology</subject><subject>Host-bacteria relationships</subject><subject>Immunologic factors</subject><subject>Inflammation</subject><subject>Insulin resistance</subject><subject>Laboratories</subject><subject>Liver diseases</subject><subject>Microbiota</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>Pediatrics</subject><subject>Rodents</subject><subject>Studies</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpFkb1uFTEQhS0EIiHQUiJL1Hvx765dRhEQpCAakOisWdtLfPGug-2b6Ha8Am0qnoVH4UnwchOoPLa-c2Y8B6HnlGy40uxV2M7zhhGq2pWQB-iYDpp2TIjPD1tNydDxQfZH6EkpW0KYFFo9RkecECU518fo9j3krz4XnCYMtoZrqN7hsEwR5hlqyntsfYwFQ_YYSkk2_CVuQr3ELhQPxePir30OdY9hWbXVlxoWiHgONqcxpArt9ddPcLtYy0G6pOX39x8QbbpMMVg8QW36GJrRve1T9GiCWPyzu_MEfXrz-uPZeXfx4e27s9OLznJNa6cVMKcFGYj2dBSO2d57IUcgahgn7p2TDrgd3Mi8laNzvWiY4hOzsu9Zz0_Qy4PvVU7fdm12s0273OYvhhHdCMoZ-U99gehNW1CqGewcijWnUgoimKKqUZsD1T5eSvaTucphhrw3lJg1MLMGZtbAzBpYE7y4a74bZ-_-4fcJ8T9IkpcL</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Schwenger, Katherine J P</creator><creator>Chen, Lina</creator><creator>Chelliah, Adeline</creator><creator>Da Silva, Hannah E</creator><creator>Teterina, Anastasia</creator><creator>Comelli, Elena M</creator><creator>Taibi, Amel</creator><creator>Arendt, Bianca M</creator><creator>Fischer, Sandra</creator><creator>Allard, Johane P</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20181001</creationdate><title>Markers of activated inflammatory cells are associated with disease severity and intestinal microbiota in adults with non‑alcoholic fatty liver disease</title><author>Schwenger, Katherine J P ; Chen, Lina ; Chelliah, Adeline ; Da Silva, Hannah E ; Teterina, Anastasia ; Comelli, Elena M ; Taibi, Amel ; Arendt, Bianca M ; Fischer, Sandra ; Allard, Johane P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-98a2d940709e1b4d2c6ee45ba087bf3edd5da3c7db2ec5bdd641b483f2c566263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alcohol</topic><topic>Architects</topic><topic>Automation</topic><topic>Biopsy</topic><topic>Care and treatment</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Fasting</topic><topic>Fatty liver</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Health aspects</topic><topic>Histology</topic><topic>Host-bacteria relationships</topic><topic>Immunologic factors</topic><topic>Inflammation</topic><topic>Insulin resistance</topic><topic>Laboratories</topic><topic>Liver diseases</topic><topic>Microbiota</topic><topic>Microbiota (Symbiotic organisms)</topic><topic>Pediatrics</topic><topic>Rodents</topic><topic>Studies</topic><toplevel>online_resources</toplevel><creatorcontrib>Schwenger, Katherine J P</creatorcontrib><creatorcontrib>Chen, Lina</creatorcontrib><creatorcontrib>Chelliah, Adeline</creatorcontrib><creatorcontrib>Da Silva, Hannah E</creatorcontrib><creatorcontrib>Teterina, Anastasia</creatorcontrib><creatorcontrib>Comelli, Elena M</creatorcontrib><creatorcontrib>Taibi, Amel</creatorcontrib><creatorcontrib>Arendt, Bianca M</creatorcontrib><creatorcontrib>Fischer, Sandra</creatorcontrib><creatorcontrib>Allard, Johane P</creatorcontrib><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>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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 China</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schwenger, Katherine J P</au><au>Chen, Lina</au><au>Chelliah, Adeline</au><au>Da Silva, Hannah E</au><au>Teterina, Anastasia</au><au>Comelli, Elena M</au><au>Taibi, Amel</au><au>Arendt, Bianca M</au><au>Fischer, Sandra</au><au>Allard, Johane P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Markers of activated inflammatory cells are associated with disease severity and intestinal microbiota in adults with non‑alcoholic fatty liver disease</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>42</volume><issue>4</issue><spage>2229</spage><epage>2237</epage><pages>2229-2237</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Several mechanisms contribute to the pathogenesis of non‑alcoholic fatty liver disease (NAFLD). The intestinal microbiota (IM) and liver immune cells (LIC) may serve a role, but there has been no previous study assessing potential associations between IM and LIC. The aim of the present study was to investigate whether there are differences in LIC markers between patients with NAFLD and healthy controls (HC), and to determine whether these markers are associated with specific IM. The present prospective, cross‑sectional study examined a cohort of adults with liver biopsy‑confirmed NAFLD and HC. Clinical and laboratory data were collected. Fecal IM was assessed by quantitative polymerase chain reaction and LIC, by immunohistochemistry. NAFLD activity score (NAS) was used for disease severity. Liver immune cell counts were increased in patients with NAFLD (n=34) vs. HC (n=8) and this was associated with disease severity. Hematopoietic cell marker cluster of differentiation (CD)45+ and Kupffer cell marker CD163+ were higher in NAFLD compared with HC, and those with an NAS ≥5 had higher levels of CD20+ cells, a marker of B cells, vs. a NAS of 0 or 1‑4. Additionally, from those patients (5 HC, 34 NAFLD), IM was measured. Specific immune cells in portal or lobular areas correlated with specific fecal IM, suggesting a potential association between IM and liver inflammation in patients with NAFLD. Specifically, Faecalibacterium prausnitzii was negatively correlated with CD45+ (r= ‑0.394; P=0.015) and CD163+ (r= ‑0.371; P=0.022) cells in the portal tract and Prevotella was negatively correlated with CD20+ (r= ‑0.353; P=0.028) cells in the liver lobule. Other taxa exhibited no correlation. In conclusion, the present study demonstrated a potential association between IM and liver inflammation in NAFLD.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30085339</pmid><doi>10.3892/ijmm.2018.3800</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alcohol Architects Automation Biopsy Care and treatment Cytokines Development and progression Fasting Fatty liver Genetic aspects Glucose Health aspects Histology Host-bacteria relationships Immunologic factors Inflammation Insulin resistance Laboratories Liver diseases Microbiota Microbiota (Symbiotic organisms) Pediatrics Rodents Studies |
title | Markers of activated inflammatory cells are associated with disease severity and intestinal microbiota in adults with non‑alcoholic fatty liver disease |
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