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
Hauptverfasser: Chen, Xiao‐Ping, Zheng, Hao, Li, Wen‐Ge, Chen, Guo‐Dong, Lu, Jin‐Xing
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container_start_page e12860
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creator Chen, Xiao‐Ping
Zheng, Hao
Li, Wen‐Ge
Chen, Guo‐Dong
Lu, Jin‐Xing
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. 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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. 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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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