Show simple item record

dc.contributor.authorAgliano, Federica
dc.contributor.authorFitzgerald, Katherine A.
dc.contributor.authorVella, Anthony T.
dc.contributor.authorRathinam, Vijay A.
dc.contributor.authorMedvedev, Andrei E.
dc.date2022-08-11T08:09:55.000
dc.date.accessioned2022-08-23T16:48:46Z
dc.date.available2022-08-23T16:48:46Z
dc.date.issued2020-01-22
dc.date.submitted2020-02-18
dc.identifier.citation<p>Agliano F, Fitzgerald KA, Vella AT, Rathinam VA, Medvedev AE. Long Non-coding RNA LincRNA-EPS Inhibits Host Defense Against <em>Listeria monocytogenes</em> Infection. Front Cell Infect Microbiol. 2020 Jan 22;9:481. doi: 10.3389/fcimb.2019.00481. PMID: 32039056; PMCID: PMC6987077. <a href="https://doi.org/10.3389/fcimb.2019.00481">Link to article on publisher's site</a></p>
dc.identifier.issn2235-2988 (Linking)
dc.identifier.doi10.3389/fcimb.2019.00481
dc.identifier.pmid32039056
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41330
dc.description.abstractLong non-coding RNAs (lncRNAs) have emerged as key regulators of gene expression in several biological systems. The long intergenic RNA-erythroid pro-survival (lincRNA-EPS) has been shown to play a critical role in restraining inflammatory gene expression. However, the function of lincRNA-EPS during bacterial infections remains unknown. Here, we demonstrate that following infection with the intracellular bacterium Listeria monocytogenes, both mouse macrophages and dendritic cells lacking lincRNA-EPS exhibit an enhanced expression of proinflammatory cytokine genes, as well as an increased expression of the inducible nitric oxide synthase (iNos) and nitric oxide (NO) production. Importantly, we found that lincRNA-EPS(-/-) mice intraperitoneally infected with L. monocytogenes exhibit lower bacterial burdens in spleen and liver and produce more NO than control mice. Furthermore, lincRNA-EPS(-/-) mice are less susceptible to a lethal dose of L. monocytogenes than wild type (WT) mice. Collectively these findings show that lincRNA-EPS suppresses host protective NO expression and impairs the host defense against L. monocytogenes infection.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=32039056&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2020 Agliano, Fitzgerald, Vella, Rathinam and Medvedev. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectListeria monocytogenes
dc.subjectinfection
dc.subjectinnate immunity
dc.subjectlincRNA-EPS
dc.subjectlncRNAs
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectBacteria
dc.subjectBacterial Infections and Mycoses
dc.subjectBacteriology
dc.subjectImmunity
dc.subjectImmunopathology
dc.subjectImmunoprophylaxis and Therapy
dc.subjectNucleic Acids, Nucleotides, and Nucleosides
dc.titleLong Non-coding RNA LincRNA-EPS Inhibits Host Defense Against Listeria monocytogenes Infection
dc.typeJournal Article
dc.source.journaltitleFrontiers in cellular and infection microbiology
dc.source.volume9
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5134&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4115
dc.identifier.contextkey16574427
refterms.dateFOA2022-08-23T16:48:46Z
html.description.abstract<p>Long non-coding RNAs (lncRNAs) have emerged as key regulators of gene expression in several biological systems. The long intergenic RNA-erythroid pro-survival (lincRNA-EPS) has been shown to play a critical role in restraining inflammatory gene expression. However, the function of lincRNA-EPS during bacterial infections remains unknown. Here, we demonstrate that following infection with the intracellular bacterium Listeria monocytogenes, both mouse macrophages and dendritic cells lacking lincRNA-EPS exhibit an enhanced expression of proinflammatory cytokine genes, as well as an increased expression of the inducible nitric oxide synthase (iNos) and nitric oxide (NO) production. Importantly, we found that lincRNA-EPS(-/-) mice intraperitoneally infected with L. monocytogenes exhibit lower bacterial burdens in spleen and liver and produce more NO than control mice. Furthermore, lincRNA-EPS(-/-) mice are less susceptible to a lethal dose of L. monocytogenes than wild type (WT) mice. Collectively these findings show that lincRNA-EPS suppresses host protective NO expression and impairs the host defense against L. monocytogenes infection.</p>
dc.identifier.submissionpathoapubs/4115
dc.contributor.departmentProgram in Innate Immunity, Division of Infectious Diseases and Immunology, Department of Medicine
dc.source.pages481


Files in this item

Thumbnail
Name:
fcimb_09_00481.pdf
Size:
1.035Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record

Copyright © 2020 Agliano, Fitzgerald, Vella, Rathinam and Medvedev. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Except where otherwise noted, this item's license is described as Copyright © 2020 Agliano, Fitzgerald, Vella, Rathinam and Medvedev. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.