Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells
Infection with bacteria such as Chlamydia pneumonia, Helicobacter pylori or Porphyromonas gingivalis may be triggering the secretion of inflammatory cytokines that leads to atherogenesis. The mechanisms by which the innate immune recognition of these pathogens could lead to atherosclerosis remain un...
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| Veröffentlicht in: | Cellular microbiology 2007-08, Vol.9 (8), p.2030-2039 |
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| creator | Triantafilou, Martha Gamper, Frederick G.J Lepper, Philipp M Mouratis, Marios Angelos Schumann, Christian Harokopakis, Evlambia Schifferle, Robert E Hajishengallis, George Triantafilou, Kathy |
| description | Infection with bacteria such as Chlamydia pneumonia, Helicobacter pylori or Porphyromonas gingivalis may be triggering the secretion of inflammatory cytokines that leads to atherogenesis. The mechanisms by which the innate immune recognition of these pathogens could lead to atherosclerosis remain unclear. In this study, using human vascular endothelial cells or HEK-293 cells engineered to express pattern-recognition receptors (PRRs), we set out to determine Toll-like receptors (TLRs) and functionally associated PRRs involved in the innate recognition of and response to lipopolysaccharide (LPS) from H. pylori or P. gingivalis. Using siRNA interference or recombinant expression of cooperating PRRs, we show that H. pylori and P. gingivalis LPS-induced cell activation is mediated through TLR2. Human vascular endothelial cell activation was found to be lipid raft-dependent and to require the formation of heterotypic receptor complexes comprising of TLR2, TLR1, CD36 and CD11b/CD18. In addition, we report that LPS from these bacterial strains are able to antagonize TLR4. This antagonistic activity of H. pylori or P. gingivalis LPS, as well as their TLR2 activation capability may be associated with their ability to contribute to atherosclerosis. |
| doi_str_mv | 10.1111/j.1462-5822.2007.00935.x |
| format | Article |
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The mechanisms by which the innate immune recognition of these pathogens could lead to atherosclerosis remain unclear. In this study, using human vascular endothelial cells or HEK-293 cells engineered to express pattern-recognition receptors (PRRs), we set out to determine Toll-like receptors (TLRs) and functionally associated PRRs involved in the innate recognition of and response to lipopolysaccharide (LPS) from H. pylori or P. gingivalis. Using siRNA interference or recombinant expression of cooperating PRRs, we show that H. pylori and P. gingivalis LPS-induced cell activation is mediated through TLR2. Human vascular endothelial cell activation was found to be lipid raft-dependent and to require the formation of heterotypic receptor complexes comprising of TLR2, TLR1, CD36 and CD11b/CD18. In addition, we report that LPS from these bacterial strains are able to antagonize TLR4. This antagonistic activity of H. pylori or P. gingivalis LPS, as well as their TLR2 activation capability may be associated with their ability to contribute to atherosclerosis.</description><identifier>ISSN: 1462-5814</identifier><identifier>EISSN: 1462-5822</identifier><identifier>DOI: 10.1111/j.1462-5822.2007.00935.x</identifier><identifier>PMID: 17419716</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Atherosclerosis - metabolism ; Atherosclerosis - microbiology ; CD11b Antigen - immunology ; CD18 Antigens - immunology ; CD36 Antigens - metabolism ; Cell Line ; Chlamydophila pneumoniae - metabolism ; Cytokines - secretion ; Endothelial Cells - metabolism ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Helicobacter pylori - metabolism ; Humans ; Lipopolysaccharides - pharmacology ; Membrane Microdomains - metabolism ; Porphyromonas gingivalis - metabolism ; Toll-Like Receptor 1 - metabolism ; Toll-Like Receptor 2 - metabolism ; Toll-Like Receptor 4 - antagonists & inhibitors ; Toll-Like Receptor 4 - metabolism</subject><ispartof>Cellular microbiology, 2007-08, Vol.9 (8), p.2030-2039</ispartof><rights>2007 The Authors; Journal compilation © 2007 Blackwell Publishing Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5335-94485fc83142ce9f19e6cc65a8b90dfa0108e36b8f507cfe39ef5cb351054e503</citedby><cites>FETCH-LOGICAL-c5335-94485fc83142ce9f19e6cc65a8b90dfa0108e36b8f507cfe39ef5cb351054e503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1462-5822.2007.00935.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1462-5822.2007.00935.x$$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/17419716$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Triantafilou, Martha</creatorcontrib><creatorcontrib>Gamper, Frederick G.J</creatorcontrib><creatorcontrib>Lepper, Philipp M</creatorcontrib><creatorcontrib>Mouratis, Marios Angelos</creatorcontrib><creatorcontrib>Schumann, Christian</creatorcontrib><creatorcontrib>Harokopakis, Evlambia</creatorcontrib><creatorcontrib>Schifferle, Robert E</creatorcontrib><creatorcontrib>Hajishengallis, George</creatorcontrib><creatorcontrib>Triantafilou, Kathy</creatorcontrib><title>Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells</title><title>Cellular microbiology</title><addtitle>Cell Microbiol</addtitle><description>Infection with bacteria such as Chlamydia pneumonia, Helicobacter pylori or Porphyromonas gingivalis may be triggering the secretion of inflammatory cytokines that leads to atherogenesis. The mechanisms by which the innate immune recognition of these pathogens could lead to atherosclerosis remain unclear. In this study, using human vascular endothelial cells or HEK-293 cells engineered to express pattern-recognition receptors (PRRs), we set out to determine Toll-like receptors (TLRs) and functionally associated PRRs involved in the innate recognition of and response to lipopolysaccharide (LPS) from H. pylori or P. gingivalis. Using siRNA interference or recombinant expression of cooperating PRRs, we show that H. pylori and P. gingivalis LPS-induced cell activation is mediated through TLR2. Human vascular endothelial cell activation was found to be lipid raft-dependent and to require the formation of heterotypic receptor complexes comprising of TLR2, TLR1, CD36 and CD11b/CD18. In addition, we report that LPS from these bacterial strains are able to antagonize TLR4. This antagonistic activity of H. pylori or P. gingivalis LPS, as well as their TLR2 activation capability may be associated with their ability to contribute to atherosclerosis.</description><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - microbiology</subject><subject>CD11b Antigen - immunology</subject><subject>CD18 Antigens - immunology</subject><subject>CD36 Antigens - metabolism</subject><subject>Cell Line</subject><subject>Chlamydophila pneumoniae - metabolism</subject><subject>Cytokines - secretion</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Helicobacter pylori - metabolism</subject><subject>Humans</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Membrane Microdomains - metabolism</subject><subject>Porphyromonas gingivalis - metabolism</subject><subject>Toll-Like Receptor 1 - metabolism</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-Like Receptor 4 - antagonists & inhibitors</subject><subject>Toll-Like Receptor 4 - metabolism</subject><issn>1462-5814</issn><issn>1462-5822</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkd2O0zAQhSMEYpeFVwCLC65IasdxfiRuUPlbqQgJdq-tqTNuXTlxsBNoeVSeBmdTLRJX-MIeab5zZuSTJITRjMWzOmSsKPNU1Hme5ZRWGaUNF9nxQXJ533h4X7PiInkSwoFSVlaMPU4uWFWwpmLlZfJ7YwY3OHsKoNQevGkxEO1dR2Dco3dB2fk2IYUQnDIwYku2oEb0Bgj0I-xcb34hudl8LV4T07eTQqKd72A0ridOz518xVbrd7wkynWDxWOcYXpizWBa4kGPITq1ZPRmt0N_J0gXpzZy2kIX3Zw_EY9hcH1Y5Pupg578gKAmC55g37q4sjVgiUJrw9PkkQYb8Nn5vUpuP7y_WX9KN18-Xq_fblIlOBdpUxS10KrmrMgVNpo1WCpVCqi3DW01UEZr5OW21oJWSiNvUAu15YJRUaCg_Cp5tfgO3n2fMIyyM2HeAHp0U5AVrXjNRRPBl_-ABzf5Pu4mc8pFSau6jFC9QCp-e_Co5eBNB_4kGZVz-PIg51zlnLGcw5d34ctjlD4_-0_bDtu_wnPaEXizAD-NxdN_G8v15-tYRPmLRa7BSdh5E-Ttt5wyHtmGFYzyP4Vkyrg</recordid><startdate>200708</startdate><enddate>200708</enddate><creator>Triantafilou, Martha</creator><creator>Gamper, Frederick G.J</creator><creator>Lepper, Philipp M</creator><creator>Mouratis, Marios Angelos</creator><creator>Schumann, Christian</creator><creator>Harokopakis, Evlambia</creator><creator>Schifferle, Robert E</creator><creator>Hajishengallis, George</creator><creator>Triantafilou, Kathy</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>Hindawi Limited</general><scope>FBQ</scope><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>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></search><sort><creationdate>200708</creationdate><title>Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells</title><author>Triantafilou, Martha ; Gamper, Frederick G.J ; Lepper, Philipp M ; Mouratis, Marios Angelos ; Schumann, Christian ; Harokopakis, Evlambia ; Schifferle, Robert E ; Hajishengallis, George ; Triantafilou, Kathy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5335-94485fc83142ce9f19e6cc65a8b90dfa0108e36b8f507cfe39ef5cb351054e503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - microbiology</topic><topic>CD11b Antigen - immunology</topic><topic>CD18 Antigens - immunology</topic><topic>CD36 Antigens - metabolism</topic><topic>Cell Line</topic><topic>Chlamydophila pneumoniae - metabolism</topic><topic>Cytokines - secretion</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - pathology</topic><topic>Helicobacter pylori - metabolism</topic><topic>Humans</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Membrane Microdomains - metabolism</topic><topic>Porphyromonas gingivalis - metabolism</topic><topic>Toll-Like Receptor 1 - metabolism</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-Like Receptor 4 - antagonists & inhibitors</topic><topic>Toll-Like Receptor 4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Triantafilou, Martha</creatorcontrib><creatorcontrib>Gamper, Frederick G.J</creatorcontrib><creatorcontrib>Lepper, Philipp M</creatorcontrib><creatorcontrib>Mouratis, Marios Angelos</creatorcontrib><creatorcontrib>Schumann, Christian</creatorcontrib><creatorcontrib>Harokopakis, Evlambia</creatorcontrib><creatorcontrib>Schifferle, Robert E</creatorcontrib><creatorcontrib>Hajishengallis, George</creatorcontrib><creatorcontrib>Triantafilou, Kathy</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><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>Triantafilou, Martha</au><au>Gamper, Frederick G.J</au><au>Lepper, Philipp M</au><au>Mouratis, Marios Angelos</au><au>Schumann, Christian</au><au>Harokopakis, Evlambia</au><au>Schifferle, Robert E</au><au>Hajishengallis, George</au><au>Triantafilou, Kathy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells</atitle><jtitle>Cellular microbiology</jtitle><addtitle>Cell Microbiol</addtitle><date>2007-08</date><risdate>2007</risdate><volume>9</volume><issue>8</issue><spage>2030</spage><epage>2039</epage><pages>2030-2039</pages><issn>1462-5814</issn><eissn>1462-5822</eissn><abstract>Infection with bacteria such as Chlamydia pneumonia, Helicobacter pylori or Porphyromonas gingivalis may be triggering the secretion of inflammatory cytokines that leads to atherogenesis. The mechanisms by which the innate immune recognition of these pathogens could lead to atherosclerosis remain unclear. In this study, using human vascular endothelial cells or HEK-293 cells engineered to express pattern-recognition receptors (PRRs), we set out to determine Toll-like receptors (TLRs) and functionally associated PRRs involved in the innate recognition of and response to lipopolysaccharide (LPS) from H. pylori or P. gingivalis. Using siRNA interference or recombinant expression of cooperating PRRs, we show that H. pylori and P. gingivalis LPS-induced cell activation is mediated through TLR2. Human vascular endothelial cell activation was found to be lipid raft-dependent and to require the formation of heterotypic receptor complexes comprising of TLR2, TLR1, CD36 and CD11b/CD18. In addition, we report that LPS from these bacterial strains are able to antagonize TLR4. This antagonistic activity of H. pylori or P. gingivalis LPS, as well as their TLR2 activation capability may be associated with their ability to contribute to atherosclerosis.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>17419716</pmid><doi>10.1111/j.1462-5822.2007.00935.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; Wiley Online Library; Alma/SFX Local Collection; EZB* |
| subjects | Atherosclerosis - metabolism Atherosclerosis - microbiology CD11b Antigen - immunology CD18 Antigens - immunology CD36 Antigens - metabolism Cell Line Chlamydophila pneumoniae - metabolism Cytokines - secretion Endothelial Cells - metabolism Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Helicobacter pylori - metabolism Humans Lipopolysaccharides - pharmacology Membrane Microdomains - metabolism Porphyromonas gingivalis - metabolism Toll-Like Receptor 1 - metabolism Toll-Like Receptor 2 - metabolism Toll-Like Receptor 4 - antagonists & inhibitors Toll-Like Receptor 4 - metabolism |
| title | Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells |
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