Pathways involved in the synergistic activation of macrophages by lipoteichoic acid and hemoglobin
Lipoteichoic acid (LTA) is a Gram-positive cell surface molecule that is found in both a cell-bound form and cell-free form in the host during an infection. Hemoglobin (Hb) can synergize with LTA, a TLR2 ligand, to potently activate macrophage innate immune responses in a TLR2- and TLR4-dependent wa...
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| description | Lipoteichoic acid (LTA) is a Gram-positive cell surface molecule that is found in both a cell-bound form and cell-free form in the host during an infection. Hemoglobin (Hb) can synergize with LTA, a TLR2 ligand, to potently activate macrophage innate immune responses in a TLR2- and TLR4-dependent way. At low levels of LTA, the presence of Hb can result in a 200-fold increase in the secretion of IL-6 following macrophage activation. Six hours after activation, the macrophage genes that are most highly up-regulated by LTA plus Hb activation compared to LTA alone are cytokines, chemokines, receptors and interferon-regulated genes. Several of these genes exhibit a unique TLR4-dependent increase in mRNA levels that continued to rise more than eight hours after stimulation. This prolonged increase in mRNA levels could be the result of an extended period of NF-κB nuclear localization and the concurrent absence of the NF-κB inhibitor, IκBα, after stimulation with LTA plus Hb. Dynasore inhibition experiments indicate that an endocytosis-dependent pathway is required for the TLR4-dependent up-regulation of IL-6 secretion following activation with LTA plus Hb. In addition, interferon-β mRNA is present after activation with LTA plus Hb, suggesting that the TRIF/TRAM-dependent pathway may be involved. Hb alone can elicit the TLR4-dependent secretion of TNF-α from macrophages, so it may be the TLR4 ligand. Hb also led to secretion of high mobility group box 1 protein (HMGB1), which synergized with LTA to increase secretion of IL-6. The activation of both the TLR2 and TLR4 pathways by LTA plus Hb leads to an enhanced innate immune response. |
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Hemoglobin (Hb) can synergize with LTA, a TLR2 ligand, to potently activate macrophage innate immune responses in a TLR2- and TLR4-dependent way. At low levels of LTA, the presence of Hb can result in a 200-fold increase in the secretion of IL-6 following macrophage activation. Six hours after activation, the macrophage genes that are most highly up-regulated by LTA plus Hb activation compared to LTA alone are cytokines, chemokines, receptors and interferon-regulated genes. Several of these genes exhibit a unique TLR4-dependent increase in mRNA levels that continued to rise more than eight hours after stimulation. This prolonged increase in mRNA levels could be the result of an extended period of NF-κB nuclear localization and the concurrent absence of the NF-κB inhibitor, IκBα, after stimulation with LTA plus Hb. Dynasore inhibition experiments indicate that an endocytosis-dependent pathway is required for the TLR4-dependent up-regulation of IL-6 secretion following activation with LTA plus Hb. In addition, interferon-β mRNA is present after activation with LTA plus Hb, suggesting that the TRIF/TRAM-dependent pathway may be involved. Hb alone can elicit the TLR4-dependent secretion of TNF-α from macrophages, so it may be the TLR4 ligand. Hb also led to secretion of high mobility group box 1 protein (HMGB1), which synergized with LTA to increase secretion of IL-6. The activation of both the TLR2 and TLR4 pathways by LTA plus Hb leads to an enhanced innate immune response.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0047333</identifier><identifier>PMID: 23071790</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acids ; Animals ; Bacteria ; Binding sites ; Biological response modifiers ; Biology ; Blotting, Western ; Bone marrow ; Cell activation ; Cell Line ; Cell surface ; Chemokines ; Comparative analysis ; Cytokines ; Endocytosis ; Experiments ; Fatty acids ; Free form ; Gene Expression Regulation - immunology ; Genes ; Health aspects ; Hemoglobin ; Hemoglobins ; Hemoglobins - metabolism ; High mobility group proteins ; HMGB1 protein ; HMGB1 Protein - metabolism ; Humans ; Immune response ; Immune system ; Immunity, Innate - immunology ; Innate immunity ; Interferon ; Interleukin 6 ; Interleukin-6 - immunology ; Laboratory animals ; Lipopolysaccharides - metabolism ; Lipoteichoic acid ; Localization ; Macrophage Activation - immunology ; Macrophages ; Mice ; Microarray Analysis ; mRNA ; Neurobiology ; Neurosciences ; NF-κB protein ; Pathways ; Phosphorylation ; Proteins ; Real-Time Polymerase Chain Reaction ; Receptors ; Reverse Transcriptase Polymerase Chain Reaction ; RNA ; Signal transduction ; Signal Transduction - immunology ; Stimulation ; Synergism ; Teichoic Acids - metabolism ; TLR2 protein ; TLR4 protein ; Toll-Like Receptor 2 - metabolism ; Toll-Like Receptor 4 - metabolism ; Toll-like receptors ; Transcription activation ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2012-10, Vol.7 (10), p.e47333-e47333</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Cox et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>2012 Cox et al 2012 Cox et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-717bc6444d78adc075d60b2ca176493713d94f663801641bb04762d4e6540d5d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468568/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468568/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23071790$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cox, Kathleen H</creatorcontrib><creatorcontrib>Cox, Michelle E</creatorcontrib><creatorcontrib>Woo-Rasberry, Virginia</creatorcontrib><creatorcontrib>Hasty, David L</creatorcontrib><title>Pathways involved in the synergistic activation of macrophages by lipoteichoic acid and hemoglobin</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Lipoteichoic acid (LTA) is a Gram-positive cell surface molecule that is found in both a cell-bound form and cell-free form in the host during an infection. Hemoglobin (Hb) can synergize with LTA, a TLR2 ligand, to potently activate macrophage innate immune responses in a TLR2- and TLR4-dependent way. At low levels of LTA, the presence of Hb can result in a 200-fold increase in the secretion of IL-6 following macrophage activation. Six hours after activation, the macrophage genes that are most highly up-regulated by LTA plus Hb activation compared to LTA alone are cytokines, chemokines, receptors and interferon-regulated genes. Several of these genes exhibit a unique TLR4-dependent increase in mRNA levels that continued to rise more than eight hours after stimulation. This prolonged increase in mRNA levels could be the result of an extended period of NF-κB nuclear localization and the concurrent absence of the NF-κB inhibitor, IκBα, after stimulation with LTA plus Hb. Dynasore inhibition experiments indicate that an endocytosis-dependent pathway is required for the TLR4-dependent up-regulation of IL-6 secretion following activation with LTA plus Hb. In addition, interferon-β mRNA is present after activation with LTA plus Hb, suggesting that the TRIF/TRAM-dependent pathway may be involved. Hb alone can elicit the TLR4-dependent secretion of TNF-α from macrophages, so it may be the TLR4 ligand. Hb also led to secretion of high mobility group box 1 protein (HMGB1), which synergized with LTA to increase secretion of IL-6. The activation of both the TLR2 and TLR4 pathways by LTA plus Hb leads to an enhanced innate immune response.</description><subject>Acids</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Binding sites</subject><subject>Biological response modifiers</subject><subject>Biology</subject><subject>Blotting, Western</subject><subject>Bone marrow</subject><subject>Cell activation</subject><subject>Cell Line</subject><subject>Cell surface</subject><subject>Chemokines</subject><subject>Comparative analysis</subject><subject>Cytokines</subject><subject>Endocytosis</subject><subject>Experiments</subject><subject>Fatty acids</subject><subject>Free form</subject><subject>Gene Expression Regulation - immunology</subject><subject>Genes</subject><subject>Health aspects</subject><subject>Hemoglobin</subject><subject>Hemoglobins</subject><subject>Hemoglobins - metabolism</subject><subject>High mobility group proteins</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - metabolism</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity, Innate - immunology</subject><subject>Innate immunity</subject><subject>Interferon</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - immunology</subject><subject>Laboratory animals</subject><subject>Lipopolysaccharides - metabolism</subject><subject>Lipoteichoic acid</subject><subject>Localization</subject><subject>Macrophage Activation - immunology</subject><subject>Macrophages</subject><subject>Mice</subject><subject>Microarray Analysis</subject><subject>mRNA</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>NF-κB protein</subject><subject>Pathways</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptors</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA</subject><subject>Signal transduction</subject><subject>Signal Transduction - immunology</subject><subject>Stimulation</subject><subject>Synergism</subject><subject>Teichoic Acids - metabolism</subject><subject>TLR2 protein</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-like receptors</subject><subject>Transcription activation</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QLgujFjPlq2twIy-LHwMKKX7fhNEnbLJlmbNLR-fdmdrrLVPZCcpGQPOdN3pNzsuw5RktMS_zu2o9DD2658b1ZIsRKSumD7BQLShacIPrwaH2SPQnhGqGCVpw_zk4IRSUuBTrN6i8Qu9-wC7ntt95tjU6LPHYmD7veDK0N0aocVLRbiNb3uW_yNajBbzpoTcjrXe7sxkdjVedvSKtz6HXembVvna9t_zR71IAL5tk0n2U_Pn74fvF5cXn1aXVxfrlQXJC4SA-qFWeM6bICrVBZaI5qogCXnInkmGrBGs5phTBnuK6TZU40M7xgSBeanmUvD7ob54Oc0hMkpoQXhSAIJWJ1ILSHa7kZ7BqGnfRg5c2GH1oJQ_LrjNSqaQToxlCDmWBIQFkDooZSQUQ6TFrvp9vGem20Mn0cwM1E5ye97WTrt5IyXhW8SgJvJoHB_xpNiHJtgzLOQW_8mN6NMeEVqXiZ0Ff_oPe7m6gWkgHbNz7dq_ai8rxglBIhKE_U8h4qDW3WVqVaamzanwW8nQUkJpo_sYUxBLn69vX_2aufc_b1EdsZcLEL3o37KgtzkB3AVHUhDKa5SzJGct8Kt9mQ-1aQUyuksBfHH3QXdFv79C8KewQG</recordid><startdate>20121010</startdate><enddate>20121010</enddate><creator>Cox, Kathleen H</creator><creator>Cox, Michelle E</creator><creator>Woo-Rasberry, Virginia</creator><creator>Hasty, David L</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>IOV</scope><scope>ISR</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>20121010</creationdate><title>Pathways involved in the synergistic activation of macrophages by lipoteichoic acid and hemoglobin</title><author>Cox, Kathleen H ; Cox, Michelle E ; Woo-Rasberry, Virginia ; Hasty, David L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-717bc6444d78adc075d60b2ca176493713d94f663801641bb04762d4e6540d5d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acids</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Binding sites</topic><topic>Biological response modifiers</topic><topic>Biology</topic><topic>Blotting, Western</topic><topic>Bone marrow</topic><topic>Cell activation</topic><topic>Cell Line</topic><topic>Cell surface</topic><topic>Chemokines</topic><topic>Comparative analysis</topic><topic>Cytokines</topic><topic>Endocytosis</topic><topic>Experiments</topic><topic>Fatty acids</topic><topic>Free form</topic><topic>Gene Expression Regulation - immunology</topic><topic>Genes</topic><topic>Health aspects</topic><topic>Hemoglobin</topic><topic>Hemoglobins</topic><topic>Hemoglobins - metabolism</topic><topic>High mobility group proteins</topic><topic>HMGB1 protein</topic><topic>HMGB1 Protein - metabolism</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity, Innate - immunology</topic><topic>Innate immunity</topic><topic>Interferon</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - immunology</topic><topic>Laboratory animals</topic><topic>Lipopolysaccharides - metabolism</topic><topic>Lipoteichoic acid</topic><topic>Localization</topic><topic>Macrophage Activation - immunology</topic><topic>Macrophages</topic><topic>Mice</topic><topic>Microarray Analysis</topic><topic>mRNA</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>NF-κB protein</topic><topic>Pathways</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Receptors</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA</topic><topic>Signal transduction</topic><topic>Signal Transduction - immunology</topic><topic>Stimulation</topic><topic>Synergism</topic><topic>Teichoic Acids - metabolism</topic><topic>TLR2 protein</topic><topic>TLR4 protein</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Toll-like receptors</topic><topic>Transcription activation</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cox, Kathleen H</creatorcontrib><creatorcontrib>Cox, Michelle E</creatorcontrib><creatorcontrib>Woo-Rasberry, Virginia</creatorcontrib><creatorcontrib>Hasty, David L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Opposing Viewpoints in Context (Gale)</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</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</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 - 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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>Cox, Kathleen H</au><au>Cox, Michelle E</au><au>Woo-Rasberry, Virginia</au><au>Hasty, David L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathways involved in the synergistic activation of macrophages by lipoteichoic acid and hemoglobin</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-10-10</date><risdate>2012</risdate><volume>7</volume><issue>10</issue><spage>e47333</spage><epage>e47333</epage><pages>e47333-e47333</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Lipoteichoic acid (LTA) is a Gram-positive cell surface molecule that is found in both a cell-bound form and cell-free form in the host during an infection. Hemoglobin (Hb) can synergize with LTA, a TLR2 ligand, to potently activate macrophage innate immune responses in a TLR2- and TLR4-dependent way. At low levels of LTA, the presence of Hb can result in a 200-fold increase in the secretion of IL-6 following macrophage activation. Six hours after activation, the macrophage genes that are most highly up-regulated by LTA plus Hb activation compared to LTA alone are cytokines, chemokines, receptors and interferon-regulated genes. Several of these genes exhibit a unique TLR4-dependent increase in mRNA levels that continued to rise more than eight hours after stimulation. This prolonged increase in mRNA levels could be the result of an extended period of NF-κB nuclear localization and the concurrent absence of the NF-κB inhibitor, IκBα, after stimulation with LTA plus Hb. Dynasore inhibition experiments indicate that an endocytosis-dependent pathway is required for the TLR4-dependent up-regulation of IL-6 secretion following activation with LTA plus Hb. In addition, interferon-β mRNA is present after activation with LTA plus Hb, suggesting that the TRIF/TRAM-dependent pathway may be involved. Hb alone can elicit the TLR4-dependent secretion of TNF-α from macrophages, so it may be the TLR4 ligand. Hb also led to secretion of high mobility group box 1 protein (HMGB1), which synergized with LTA to increase secretion of IL-6. The activation of both the TLR2 and TLR4 pathways by LTA plus Hb leads to an enhanced innate immune response.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23071790</pmid><doi>10.1371/journal.pone.0047333</doi><tpages>e47333</tpages><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acids Animals Bacteria Binding sites Biological response modifiers Biology Blotting, Western Bone marrow Cell activation Cell Line Cell surface Chemokines Comparative analysis Cytokines Endocytosis Experiments Fatty acids Free form Gene Expression Regulation - immunology Genes Health aspects Hemoglobin Hemoglobins Hemoglobins - metabolism High mobility group proteins HMGB1 protein HMGB1 Protein - metabolism Humans Immune response Immune system Immunity, Innate - immunology Innate immunity Interferon Interleukin 6 Interleukin-6 - immunology Laboratory animals Lipopolysaccharides - metabolism Lipoteichoic acid Localization Macrophage Activation - immunology Macrophages Mice Microarray Analysis mRNA Neurobiology Neurosciences NF-κB protein Pathways Phosphorylation Proteins Real-Time Polymerase Chain Reaction Receptors Reverse Transcriptase Polymerase Chain Reaction RNA Signal transduction Signal Transduction - immunology Stimulation Synergism Teichoic Acids - metabolism TLR2 protein TLR4 protein Toll-Like Receptor 2 - metabolism Toll-Like Receptor 4 - metabolism Toll-like receptors Transcription activation Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Pathways involved in the synergistic activation of macrophages by lipoteichoic acid and hemoglobin |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T16%3A03%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Pathways%20involved%20in%20the%20synergistic%20activation%20of%20macrophages%20by%20lipoteichoic%20acid%20and%20hemoglobin&rft.jtitle=PloS%20one&rft.au=Cox,%20Kathleen%20H&rft.date=2012-10-10&rft.volume=7&rft.issue=10&rft.spage=e47333&rft.epage=e47333&rft.pages=e47333-e47333&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0047333&rft_dat=%3Cgale_plos_%3EA543329936%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1326559200&rft_id=info:pmid/23071790&rft_galeid=A543329936&rft_doaj_id=oai_doaj_org_article_dcff9adfe3e149409a7ba03e33929dcf&rfr_iscdi=true |