Bacteria‐induced susceptibility to Candida albicans super‐infection in mice via monocyte methyltransferase Setdb2
Systemic bacterial infections are prone to secondary Candida albicans super‐infection. However, the molecular mechanisms involved remain poorly understood. In this study, a model comprising sublethal cecal ligation and puncture plus C. albicans intravenous injection was applied to mimic the situatio...
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Veröffentlicht in: | Cellular microbiology 2018-09, Vol.20 (9), p.e12860-n/a |
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description | Systemic bacterial infections are prone to secondary Candida albicans super‐infection. However, the molecular mechanisms involved remain poorly understood. In this study, a model comprising sublethal cecal ligation and puncture plus C. albicans intravenous injection was applied to mimic the situation in super‐infection. Compared with mice without systemic bacterial infection, mice with systemic bacterial infection had lower antifungal gene expression (including Il1b, Tnf, Il6, Ifnb, Ifng, Cxcl1, and Ccr2) in monocytes and less inflammatory monocytes and neutrophils infiltrating into the kidney when challenged with C. albicans. Further, lentivirus‐mediated Setdb2‐knockout and overexpression experiments verified that Setdb2 levels in monocytes correlated negatively with antifungal gene expression and survival rates. Transcriptional repression was probably achieved by Setdb2 through H3 methylation at lysine 9 in promoter regions of these antifungal genes. |
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However, the molecular mechanisms involved remain poorly understood. In this study, a model comprising sublethal cecal ligation and puncture plus C. albicans intravenous injection was applied to mimic the situation in super‐infection. Compared with mice without systemic bacterial infection, mice with systemic bacterial infection had lower antifungal gene expression (including Il1b, Tnf, Il6, Ifnb, Ifng, Cxcl1, and Ccr2) in monocytes and less inflammatory monocytes and neutrophils infiltrating into the kidney when challenged with C. albicans. Further, lentivirus‐mediated Setdb2‐knockout and overexpression experiments verified that Setdb2 levels in monocytes correlated negatively with antifungal gene expression and survival rates. Transcriptional repression was probably achieved by Setdb2 through H3 methylation at lysine 9 in promoter regions of these antifungal genes.</description><identifier>ISSN: 1462-5814</identifier><identifier>EISSN: 1462-5822</identifier><identifier>DOI: 10.1111/cmi.12860</identifier><identifier>PMID: 29749709</identifier><language>eng</language><publisher>England: Hindawi Limited</publisher><subject>antifungal gene ; Bacteria ; Bacterial infections ; C. albicans super‐infection ; Candida albicans ; CCR2 protein ; Cecum ; DNA methylation ; Fungicides ; Gene expression ; Gene silencing ; Infections ; Inflammation ; Interleukin 1 ; Interleukin 6 ; Intravenous administration ; Kidneys ; Leukocytes (neutrophilic) ; Lysine ; Methyltransferase ; Mice ; Molecular modelling ; Monocyte chemoattractant protein 1 ; Monocytes ; Setdb2 ; systemic bacterial infection ; Tumor necrosis factor</subject><ispartof>Cellular microbiology, 2018-09, Vol.20 (9), p.e12860-n/a</ispartof><rights>2018 John Wiley & Sons Ltd</rights><rights>2018 John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-bb054c1defba2eaa9c252cbbfe12fbc1e4b1e43e114445b534622991b3fcfdf03</citedby><cites>FETCH-LOGICAL-c3530-bb054c1defba2eaa9c252cbbfe12fbc1e4b1e43e114445b534622991b3fcfdf03</cites><orcidid>0000-0002-3435-9754</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fcmi.12860$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fcmi.12860$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29749709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Xiao‐Ping</creatorcontrib><creatorcontrib>Zheng, Hao</creatorcontrib><creatorcontrib>Li, Wen‐Ge</creatorcontrib><creatorcontrib>Chen, Guo‐Dong</creatorcontrib><creatorcontrib>Lu, Jin‐Xing</creatorcontrib><title>Bacteria‐induced susceptibility to Candida albicans super‐infection in mice via monocyte methyltransferase Setdb2</title><title>Cellular microbiology</title><addtitle>Cell Microbiol</addtitle><description>Systemic bacterial infections are prone to secondary Candida albicans super‐infection. However, the molecular mechanisms involved remain poorly understood. In this study, a model comprising sublethal cecal ligation and puncture plus C. albicans intravenous injection was applied to mimic the situation in super‐infection. Compared with mice without systemic bacterial infection, mice with systemic bacterial infection had lower antifungal gene expression (including Il1b, Tnf, Il6, Ifnb, Ifng, Cxcl1, and Ccr2) in monocytes and less inflammatory monocytes and neutrophils infiltrating into the kidney when challenged with C. albicans. Further, lentivirus‐mediated Setdb2‐knockout and overexpression experiments verified that Setdb2 levels in monocytes correlated negatively with antifungal gene expression and survival rates. Transcriptional repression was probably achieved by Setdb2 through H3 methylation at lysine 9 in promoter regions of these antifungal genes.</description><subject>antifungal gene</subject><subject>Bacteria</subject><subject>Bacterial infections</subject><subject>C. albicans super‐infection</subject><subject>Candida albicans</subject><subject>CCR2 protein</subject><subject>Cecum</subject><subject>DNA methylation</subject><subject>Fungicides</subject><subject>Gene expression</subject><subject>Gene silencing</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Interleukin 1</subject><subject>Interleukin 6</subject><subject>Intravenous administration</subject><subject>Kidneys</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lysine</subject><subject>Methyltransferase</subject><subject>Mice</subject><subject>Molecular modelling</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Setdb2</subject><subject>systemic bacterial infection</subject><subject>Tumor necrosis factor</subject><issn>1462-5814</issn><issn>1462-5822</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp10btKBDEUBuAgiq6rhS8gARstVnOb2UmpizdYsVDrIcmcYGQua5JRpvMRfEafxLirFoKBkBTf-cnJQWiPkmOa1olp3DFlRU7W0IiKnE2ygrH13zsVW2g7hCdCaD6ldBNtMTkVckrkCPVnykTwTn28vbu26g1UOPTBwCI67WoXBxw7PFNt5SqFVa2dUW1IZAF-WWLBRNe12LW4cQbwi1O46drODBFwA_FxqKNPJRa8CoDvIFaa7aANq-oAu9_nGD1cnN_Pribz28vr2el8YnjGyURrkglDK7BaMVBKGpYxo7UFyqw2FIROmwOlQohMZzz1y6SkmltjK0v4GB2uche-e-4hxLJxqbe6Vi10fSgZ4QXLZZHzRA_-0Keu9216XVKSF7IQlCV1tFLGdyF4sOXCu0b5oaSk_JpFmWZRLmeR7P53Yq8bqH7lz-cncLICr66G4f-kcnZzvYr8BNXTlzs</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Chen, Xiao‐Ping</creator><creator>Zheng, Hao</creator><creator>Li, Wen‐Ge</creator><creator>Chen, Guo‐Dong</creator><creator>Lu, Jin‐Xing</creator><general>Hindawi Limited</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3435-9754</orcidid></search><sort><creationdate>201809</creationdate><title>Bacteria‐induced susceptibility to Candida albicans super‐infection in mice via monocyte methyltransferase Setdb2</title><author>Chen, Xiao‐Ping ; Zheng, Hao ; Li, Wen‐Ge ; Chen, Guo‐Dong ; Lu, Jin‐Xing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3530-bb054c1defba2eaa9c252cbbfe12fbc1e4b1e43e114445b534622991b3fcfdf03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>antifungal gene</topic><topic>Bacteria</topic><topic>Bacterial infections</topic><topic>C. albicans super‐infection</topic><topic>Candida albicans</topic><topic>CCR2 protein</topic><topic>Cecum</topic><topic>DNA methylation</topic><topic>Fungicides</topic><topic>Gene expression</topic><topic>Gene silencing</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Interleukin 1</topic><topic>Interleukin 6</topic><topic>Intravenous administration</topic><topic>Kidneys</topic><topic>Leukocytes (neutrophilic)</topic><topic>Lysine</topic><topic>Methyltransferase</topic><topic>Mice</topic><topic>Molecular modelling</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Setdb2</topic><topic>systemic bacterial infection</topic><topic>Tumor necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Xiao‐Ping</creatorcontrib><creatorcontrib>Zheng, Hao</creatorcontrib><creatorcontrib>Li, Wen‐Ge</creatorcontrib><creatorcontrib>Chen, Guo‐Dong</creatorcontrib><creatorcontrib>Lu, Jin‐Xing</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Xiao‐Ping</au><au>Zheng, Hao</au><au>Li, Wen‐Ge</au><au>Chen, Guo‐Dong</au><au>Lu, Jin‐Xing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bacteria‐induced susceptibility to Candida albicans super‐infection in mice via monocyte methyltransferase Setdb2</atitle><jtitle>Cellular microbiology</jtitle><addtitle>Cell Microbiol</addtitle><date>2018-09</date><risdate>2018</risdate><volume>20</volume><issue>9</issue><spage>e12860</spage><epage>n/a</epage><pages>e12860-n/a</pages><issn>1462-5814</issn><eissn>1462-5822</eissn><abstract>Systemic bacterial infections are prone to secondary Candida albicans super‐infection. However, the molecular mechanisms involved remain poorly understood. In this study, a model comprising sublethal cecal ligation and puncture plus C. albicans intravenous injection was applied to mimic the situation in super‐infection. Compared with mice without systemic bacterial infection, mice with systemic bacterial infection had lower antifungal gene expression (including Il1b, Tnf, Il6, Ifnb, Ifng, Cxcl1, and Ccr2) in monocytes and less inflammatory monocytes and neutrophils infiltrating into the kidney when challenged with C. albicans. Further, lentivirus‐mediated Setdb2‐knockout and overexpression experiments verified that Setdb2 levels in monocytes correlated negatively with antifungal gene expression and survival rates. Transcriptional repression was probably achieved by Setdb2 through H3 methylation at lysine 9 in promoter regions of these antifungal genes.</abstract><cop>England</cop><pub>Hindawi Limited</pub><pmid>29749709</pmid><doi>10.1111/cmi.12860</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-3435-9754</orcidid></addata></record> |
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subjects | antifungal gene Bacteria Bacterial infections C. albicans super‐infection Candida albicans CCR2 protein Cecum DNA methylation Fungicides Gene expression Gene silencing Infections Inflammation Interleukin 1 Interleukin 6 Intravenous administration Kidneys Leukocytes (neutrophilic) Lysine Methyltransferase Mice Molecular modelling Monocyte chemoattractant protein 1 Monocytes Setdb2 systemic bacterial infection Tumor necrosis factor |
title | Bacteria‐induced susceptibility to Candida albicans super‐infection in mice via monocyte methyltransferase Setdb2 |
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