Roles of TLR/MyD88/MAPK/NF-κB Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection
Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and...
Gespeichert in:
| Veröffentlicht in: | PloS one 2015-08, Vol.10 (8), p.e0136947-e0136947 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0136947 |
|---|---|
| container_issue | 8 |
| container_start_page | e0136947 |
| container_title | PloS one |
| container_volume | 10 |
| creator | Zou, Jun Shankar, Nathan |
| description | Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and also have an important role in mediating chromosomal instability and promoting colon cancer during high-level enterococcal colonization in genetically susceptible mice. However, the molecular mechanisms involved in the interaction of macrophages with enterococci during infection are not fully understood. In this study, using BMDM and RAW264.7 macrophages we show that enterococcal infection activates ERK, JNK and p38 MAPK as well as NF-κB, and drives polarization of macrophages towards the M1 phenotype. Inhibition of NF-κB activation significantly reduced the expression of TNF-α and IL-1β, as did the inhibition of ERK, JNK and p38 MAPK, although to differing extent. Enterococci-induced activation of these pathways and subsequent cytokine expression was contact dependent, modest compared to activation by E. coli and, required the adaptor protein MyD88. Phagocytosis of enterococci by macrophages was enhanced by preopsonization with E. faecalis antiserum and involved the ERK and JNK signaling pathways, with the adaptor protein MyD88 as an important mediator. This study of the interaction of macrophages with enterococci could provide a foundation for studying the pathogenesis of infection by this opportunistic pathogen and to developing new therapeutic approaches to combat enterococcal infection. |
| doi_str_mv | 10.1371/journal.pone.0136947 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1708482610</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_b9bd851015fa4761aaac95b1cc448a1e</doaj_id><sourcerecordid>1708901245</sourcerecordid><originalsourceid>FETCH-LOGICAL-c456t-2e51fdd4556cd15335a1382fc18b1bc907a04c529fd9ce2d819ac1155ca662823</originalsourceid><addsrcrecordid>eNptUstuEzEUHSEQLYU_QGCJDZskfo9ng1RCChEpRKGsrTsez8RhYgd7AuRv-A4-gm9iQtKqRaxs-Z7HPdbJsqcEDwnLyWgVttFDO9wEb4eYMFnw_F52SgpGB5Jidv_W_SR7lNIKY8GUlA-zEyoZyTlTp9nPRWhtQqFGV7PF6HL3RqnR5fn8_ejDxeD3r9fok2t6E-cbNIdu-R12CTmPuqVFC9tsW-hc8Hv2fAlNMLsuJJcQ-ArNY3C-bmG9hi7EHRr3sy_OWzT5sYk2pT2vV1rY1AdIFnUBTYaoBmt6u4SmvrZmL_44e1BDm-yT43mWfb6YXI3fDWYf307H57OB4UJ2A2oFqauKCyFNRQRjAghTtDZElaQ0Bc4BcyNoUVeFsbRSpABDiBAGpKSKsrPs-UF304akj5-bNMmx4opKgnvE9ICoAqz0Jro1xJ0O4PTfhxAbDbFzprW6LMpKCYKJqIHnkgCAKURJjOFcAbG91quj27Zc28pY30Vo74jenXi31E34pvuAVOasF3h5FIjh69amTq9dMrZtwduwPexdYEK56KEv_oH-Px0_oEwMKUVb3yxDsN4X7pql94XTx8L1tGe3g9yQrhvG_gDKbtXp</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1708482610</pqid></control><display><type>article</type><title>Roles of TLR/MyD88/MAPK/NF-κB Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Zou, Jun ; Shankar, Nathan</creator><contributor>Bayry, Jagadeesh</contributor><creatorcontrib>Zou, Jun ; Shankar, Nathan ; Bayry, Jagadeesh</creatorcontrib><description>Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and also have an important role in mediating chromosomal instability and promoting colon cancer during high-level enterococcal colonization in genetically susceptible mice. However, the molecular mechanisms involved in the interaction of macrophages with enterococci during infection are not fully understood. In this study, using BMDM and RAW264.7 macrophages we show that enterococcal infection activates ERK, JNK and p38 MAPK as well as NF-κB, and drives polarization of macrophages towards the M1 phenotype. Inhibition of NF-κB activation significantly reduced the expression of TNF-α and IL-1β, as did the inhibition of ERK, JNK and p38 MAPK, although to differing extent. Enterococci-induced activation of these pathways and subsequent cytokine expression was contact dependent, modest compared to activation by E. coli and, required the adaptor protein MyD88. Phagocytosis of enterococci by macrophages was enhanced by preopsonization with E. faecalis antiserum and involved the ERK and JNK signaling pathways, with the adaptor protein MyD88 as an important mediator. This study of the interaction of macrophages with enterococci could provide a foundation for studying the pathogenesis of infection by this opportunistic pathogen and to developing new therapeutic approaches to combat enterococcal infection.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0136947</identifier><identifier>PMID: 26317438</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Bacteria ; Bacterial infections ; Bacterial proteins ; Bone marrow ; Cell activation ; Cell Line ; Colon ; Colon cancer ; Colonization ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Disease control ; Disease Models, Animal ; E coli ; Enterococcus faecalis ; Enterococcus faecalis - immunology ; Enterococcus faecalis - isolation & purification ; Enterococcus faecalis - pathogenicity ; Gastrointestinal tract ; Gene expression ; Genomic instability ; Gram-Positive Bacterial Infections - genetics ; Gram-Positive Bacterial Infections - immunology ; Gram-Positive Bacterial Infections - metabolism ; Gram-Positive Bacterial Infections - microbiology ; Health sciences ; IL-1β ; Infections ; Inflammation ; Inhibition ; Kinases ; Laboratory animals ; Macrophages ; Macrophages - immunology ; Macrophages - microbiology ; Macrophages - physiology ; MAP kinase ; MAP Kinase Signaling System ; Mice ; Molecular chains ; Molecular modelling ; MyD88 protein ; Myeloid Differentiation Factor 88 - metabolism ; NF-kappa B - metabolism ; NF-κB protein ; Opportunist infection ; Pathogenesis ; Pathogens ; Phagocytosis ; Pharmaceutical sciences ; Phenotypes ; Proteins ; Sepsis ; Signal transduction ; Signaling ; Stability ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2015-08, Vol.10 (8), p.e0136947-e0136947</ispartof><rights>2015 Zou, Shankar. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Zou, Shankar 2015 Zou, Shankar</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-2e51fdd4556cd15335a1382fc18b1bc907a04c529fd9ce2d819ac1155ca662823</citedby><cites>FETCH-LOGICAL-c456t-2e51fdd4556cd15335a1382fc18b1bc907a04c529fd9ce2d819ac1155ca662823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552673/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552673/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26317438$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bayry, Jagadeesh</contributor><creatorcontrib>Zou, Jun</creatorcontrib><creatorcontrib>Shankar, Nathan</creatorcontrib><title>Roles of TLR/MyD88/MAPK/NF-κB Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and also have an important role in mediating chromosomal instability and promoting colon cancer during high-level enterococcal colonization in genetically susceptible mice. However, the molecular mechanisms involved in the interaction of macrophages with enterococci during infection are not fully understood. In this study, using BMDM and RAW264.7 macrophages we show that enterococcal infection activates ERK, JNK and p38 MAPK as well as NF-κB, and drives polarization of macrophages towards the M1 phenotype. Inhibition of NF-κB activation significantly reduced the expression of TNF-α and IL-1β, as did the inhibition of ERK, JNK and p38 MAPK, although to differing extent. Enterococci-induced activation of these pathways and subsequent cytokine expression was contact dependent, modest compared to activation by E. coli and, required the adaptor protein MyD88. Phagocytosis of enterococci by macrophages was enhanced by preopsonization with E. faecalis antiserum and involved the ERK and JNK signaling pathways, with the adaptor protein MyD88 as an important mediator. This study of the interaction of macrophages with enterococci could provide a foundation for studying the pathogenesis of infection by this opportunistic pathogen and to developing new therapeutic approaches to combat enterococcal infection.</description><subject>Animals</subject><subject>Bacteria</subject><subject>Bacterial infections</subject><subject>Bacterial proteins</subject><subject>Bone marrow</subject><subject>Cell activation</subject><subject>Cell Line</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colonization</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Disease control</subject><subject>Disease Models, Animal</subject><subject>E coli</subject><subject>Enterococcus faecalis</subject><subject>Enterococcus faecalis - immunology</subject><subject>Enterococcus faecalis - isolation & purification</subject><subject>Enterococcus faecalis - pathogenicity</subject><subject>Gastrointestinal tract</subject><subject>Gene expression</subject><subject>Genomic instability</subject><subject>Gram-Positive Bacterial Infections - genetics</subject><subject>Gram-Positive Bacterial Infections - immunology</subject><subject>Gram-Positive Bacterial Infections - metabolism</subject><subject>Gram-Positive Bacterial Infections - microbiology</subject><subject>Health sciences</subject><subject>IL-1β</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Inhibition</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - microbiology</subject><subject>Macrophages - physiology</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System</subject><subject>Mice</subject><subject>Molecular chains</subject><subject>Molecular modelling</subject><subject>MyD88 protein</subject><subject>Myeloid Differentiation Factor 88 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Opportunist infection</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Phagocytosis</subject><subject>Pharmaceutical sciences</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Sepsis</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Stability</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUstuEzEUHSEQLYU_QGCJDZskfo9ng1RCChEpRKGsrTsez8RhYgd7AuRv-A4-gm9iQtKqRaxs-Z7HPdbJsqcEDwnLyWgVttFDO9wEb4eYMFnw_F52SgpGB5Jidv_W_SR7lNIKY8GUlA-zEyoZyTlTp9nPRWhtQqFGV7PF6HL3RqnR5fn8_ejDxeD3r9fok2t6E-cbNIdu-R12CTmPuqVFC9tsW-hc8Hv2fAlNMLsuJJcQ-ArNY3C-bmG9hi7EHRr3sy_OWzT5sYk2pT2vV1rY1AdIFnUBTYaoBmt6u4SmvrZmL_44e1BDm-yT43mWfb6YXI3fDWYf307H57OB4UJ2A2oFqauKCyFNRQRjAghTtDZElaQ0Bc4BcyNoUVeFsbRSpABDiBAGpKSKsrPs-UF304akj5-bNMmx4opKgnvE9ICoAqz0Jro1xJ0O4PTfhxAbDbFzprW6LMpKCYKJqIHnkgCAKURJjOFcAbG91quj27Zc28pY30Vo74jenXi31E34pvuAVOasF3h5FIjh69amTq9dMrZtwduwPexdYEK56KEv_oH-Px0_oEwMKUVb3yxDsN4X7pql94XTx8L1tGe3g9yQrhvG_gDKbtXp</recordid><startdate>20150828</startdate><enddate>20150828</enddate><creator>Zou, Jun</creator><creator>Shankar, Nathan</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150828</creationdate><title>Roles of TLR/MyD88/MAPK/NF-κB Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection</title><author>Zou, Jun ; Shankar, Nathan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-2e51fdd4556cd15335a1382fc18b1bc907a04c529fd9ce2d819ac1155ca662823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Bacteria</topic><topic>Bacterial infections</topic><topic>Bacterial proteins</topic><topic>Bone marrow</topic><topic>Cell activation</topic><topic>Cell Line</topic><topic>Colon</topic><topic>Colon cancer</topic><topic>Colonization</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Disease control</topic><topic>Disease Models, Animal</topic><topic>E coli</topic><topic>Enterococcus faecalis</topic><topic>Enterococcus faecalis - immunology</topic><topic>Enterococcus faecalis - isolation & purification</topic><topic>Enterococcus faecalis - pathogenicity</topic><topic>Gastrointestinal tract</topic><topic>Gene expression</topic><topic>Genomic instability</topic><topic>Gram-Positive Bacterial Infections - genetics</topic><topic>Gram-Positive Bacterial Infections - immunology</topic><topic>Gram-Positive Bacterial Infections - metabolism</topic><topic>Gram-Positive Bacterial Infections - microbiology</topic><topic>Health sciences</topic><topic>IL-1β</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Inhibition</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - microbiology</topic><topic>Macrophages - physiology</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System</topic><topic>Mice</topic><topic>Molecular chains</topic><topic>Molecular modelling</topic><topic>MyD88 protein</topic><topic>Myeloid Differentiation Factor 88 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Opportunist infection</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Phagocytosis</topic><topic>Pharmaceutical sciences</topic><topic>Phenotypes</topic><topic>Proteins</topic><topic>Sepsis</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Stability</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zou, Jun</creatorcontrib><creatorcontrib>Shankar, Nathan</creatorcontrib><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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zou, Jun</au><au>Shankar, Nathan</au><au>Bayry, Jagadeesh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles of TLR/MyD88/MAPK/NF-κB Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-08-28</date><risdate>2015</risdate><volume>10</volume><issue>8</issue><spage>e0136947</spage><epage>e0136947</epage><pages>e0136947-e0136947</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and also have an important role in mediating chromosomal instability and promoting colon cancer during high-level enterococcal colonization in genetically susceptible mice. However, the molecular mechanisms involved in the interaction of macrophages with enterococci during infection are not fully understood. In this study, using BMDM and RAW264.7 macrophages we show that enterococcal infection activates ERK, JNK and p38 MAPK as well as NF-κB, and drives polarization of macrophages towards the M1 phenotype. Inhibition of NF-κB activation significantly reduced the expression of TNF-α and IL-1β, as did the inhibition of ERK, JNK and p38 MAPK, although to differing extent. Enterococci-induced activation of these pathways and subsequent cytokine expression was contact dependent, modest compared to activation by E. coli and, required the adaptor protein MyD88. Phagocytosis of enterococci by macrophages was enhanced by preopsonization with E. faecalis antiserum and involved the ERK and JNK signaling pathways, with the adaptor protein MyD88 as an important mediator. This study of the interaction of macrophages with enterococci could provide a foundation for studying the pathogenesis of infection by this opportunistic pathogen and to developing new therapeutic approaches to combat enterococcal infection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26317438</pmid><doi>10.1371/journal.pone.0136947</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-08, Vol.10 (8), p.e0136947-e0136947 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1708482610 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Bacteria Bacterial infections Bacterial proteins Bone marrow Cell activation Cell Line Colon Colon cancer Colonization Cytokines Cytokines - genetics Cytokines - metabolism Disease control Disease Models, Animal E coli Enterococcus faecalis Enterococcus faecalis - immunology Enterococcus faecalis - isolation & purification Enterococcus faecalis - pathogenicity Gastrointestinal tract Gene expression Genomic instability Gram-Positive Bacterial Infections - genetics Gram-Positive Bacterial Infections - immunology Gram-Positive Bacterial Infections - metabolism Gram-Positive Bacterial Infections - microbiology Health sciences IL-1β Infections Inflammation Inhibition Kinases Laboratory animals Macrophages Macrophages - immunology Macrophages - microbiology Macrophages - physiology MAP kinase MAP Kinase Signaling System Mice Molecular chains Molecular modelling MyD88 protein Myeloid Differentiation Factor 88 - metabolism NF-kappa B - metabolism NF-κB protein Opportunist infection Pathogenesis Pathogens Phagocytosis Pharmaceutical sciences Phenotypes Proteins Sepsis Signal transduction Signaling Stability Tumor necrosis factor-α |
| title | Roles of TLR/MyD88/MAPK/NF-κB Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-13T14%3A02%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Roles%20of%20TLR/MyD88/MAPK/NF-%CE%BAB%20Signaling%20Pathways%20in%20the%20Regulation%20of%20Phagocytosis%20and%20Proinflammatory%20Cytokine%20Expression%20in%20Response%20to%20E.%20faecalis%20Infection&rft.jtitle=PloS%20one&rft.au=Zou,%20Jun&rft.date=2015-08-28&rft.volume=10&rft.issue=8&rft.spage=e0136947&rft.epage=e0136947&rft.pages=e0136947-e0136947&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0136947&rft_dat=%3Cproquest_plos_%3E1708901245%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1708482610&rft_id=info:pmid/26317438&rft_doaj_id=oai_doaj_org_article_b9bd851015fa4761aaac95b1cc448a1e&rfr_iscdi=true |