Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis
Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, in...
Gespeichert in:
| Veröffentlicht in: | PloS one 2017-02, Vol.12 (2), p.e0172773-e0172773 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0172773 |
|---|---|
| container_issue | 2 |
| container_start_page | e0172773 |
| container_title | PloS one |
| container_volume | 12 |
| creator | Køllgaard, Tania Enevold, Christian Bendtzen, Klaus Hansen, Peter R Givskov, Michael Holmstrup, Palle Nielsen, Claus H |
| description | Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, including Porphyromonas gingivalis, have been found in atherosclerotic plaques in humans and mice. We aimed to determine whether cholesterol crystals (CHCs) and oral bacteria synergize in the stimulation of human monocytes. Incubation of human monocytes with CHCs induced secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-8. Moreover, CHCs markedly enhanced secretion of IL-1β by monocytes stimulated with the toll-like receptor (TLR) 4 agonist Escherichia coli lipopolysaccharide (LPS), and the TLR2 agonist Staphylococcus aureus lipoteichoic acid. Notably, CHCs also enhanced IL-1β secretion induced by P. gingivalis LPS and IL-1β secretion induced by whole P. gingivalis bacteria. This enhancement was abrogated by the NLRP3 inflammasome inhibitors Z-YVAD-FMK and glibenclamide. CHCs had no effect on cytokine production induced by P. gingivalis gingipains. Taken together, our findings support that CHCs, via stimulation of NLRP3 inflammasomes, act in synergy with the periodontal pathogen P. gingivalis to promote monocyte secretion of pro-atherogenic cytokines. |
| doi_str_mv | 10.1371/journal.pone.0172773 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1871803022</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A482540552</galeid><doaj_id>oai_doaj_org_article_981f215c1fe94b74aba9e7ee82ebcb09</doaj_id><sourcerecordid>A482540552</sourcerecordid><originalsourceid>FETCH-LOGICAL-c791t-8f5582824d8392067599d7daa50c6674d02ef9f70137dd9fa704b6bad251ddb33</originalsourceid><addsrcrecordid>eNqNU01v1DAQjRCIlsI_QGAJCcEhi-3EcXJBqio-Kq1UVApXy7EniUtiL7ZTsb-HP4q33Va7qIcqBzv2e88zb2ay7CXBC1Jw8uHSzd7KcbFyFhaYcMp58Sg7JE1B84ri4vHO_iB7FsIlxqyoq-ppdkBrWjBcVIfZ35PBjRAieDci5dchyjEgsIO0CtDF8pzmSFq92ZX5BNrICBqtvMuN7UY5TTI6v0ZqHd0vYwF5CCmgAAG5Dk3OunSTfqJDcYANT6bVux6sUch5OaJWqvS6mSf0zfnVsPYu0WRAvbG9uZKjCc-zJ12KCl5s16Psx-dPFydf8-XZl9OT42WueENiXneM1SmzUtdFQ3HFWdNorqVkWFUVLzWm0DUdx8k-rZtOcly2VSs1ZUTrtiiOstc3uqvRBbH1NwhSc1LjAlOaEKc3CO3kpVh5M0m_Fk4acX3gfC-kj0aNIJqadJQwRTpoypaXspUNcICaQqta3CStj9vX5jYZq8DGZMee6P6NNYPo3ZVgBWWMsiTwbivg3e851VBMJigYR2nBzddx85ph0jwIShkvMduk-OY_6P1GbFG9TLmmVnApRLURFcdlTVmSutZa3INKn4bJqNS3nUnne4T3e4SEifAn9nIOQZx-P3849uznPvbtDnYAOcYhuHGOJvXqPrC8ASrvQvDQ3dWDYLEZu1s3xGbsxHbsEu3Vbi3vSLdzVvwDIW4q1A</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1871803022</pqid></control><display><type>article</type><title>Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Public Library of Science (PLoS)</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Køllgaard, Tania ; Enevold, Christian ; Bendtzen, Klaus ; Hansen, Peter R ; Givskov, Michael ; Holmstrup, Palle ; Nielsen, Claus H</creator><contributor>Amar, Salomon</contributor><creatorcontrib>Køllgaard, Tania ; Enevold, Christian ; Bendtzen, Klaus ; Hansen, Peter R ; Givskov, Michael ; Holmstrup, Palle ; Nielsen, Claus H ; Amar, Salomon</creatorcontrib><description>Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, including Porphyromonas gingivalis, have been found in atherosclerotic plaques in humans and mice. We aimed to determine whether cholesterol crystals (CHCs) and oral bacteria synergize in the stimulation of human monocytes. Incubation of human monocytes with CHCs induced secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-8. Moreover, CHCs markedly enhanced secretion of IL-1β by monocytes stimulated with the toll-like receptor (TLR) 4 agonist Escherichia coli lipopolysaccharide (LPS), and the TLR2 agonist Staphylococcus aureus lipoteichoic acid. Notably, CHCs also enhanced IL-1β secretion induced by P. gingivalis LPS and IL-1β secretion induced by whole P. gingivalis bacteria. This enhancement was abrogated by the NLRP3 inflammasome inhibitors Z-YVAD-FMK and glibenclamide. CHCs had no effect on cytokine production induced by P. gingivalis gingipains. Taken together, our findings support that CHCs, via stimulation of NLRP3 inflammasomes, act in synergy with the periodontal pathogen P. gingivalis to promote monocyte secretion of pro-atherogenic cytokines.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0172773</identifier><identifier>PMID: 28235036</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Anaerobic bacteria ; Animals ; Arteriosclerosis ; Atheroembolism ; Atherosclerosis ; Atherosclerosis - complications ; Atherosclerosis - metabolism ; Atherosclerosis - microbiology ; Bacteria ; Biology and Life Sciences ; Blood & organ donations ; Cardiovascular disease ; Cardiovascular diseases ; Cholesterol ; Cholesterol - chemistry ; Cholesterol - metabolism ; Crystals ; Cytokines ; Dentistry ; E coli ; Epidemiology ; Escherichia coli ; Fibroblasts ; Glibenclamide ; Gram-positive bacteria ; Hospitals ; Humans ; Immune system ; Inflammasomes ; Inflammasomes - drug effects ; Inflammasomes - metabolism ; Inflammation ; Interleukin 6 ; Interleukin 8 ; Interleukin-1beta - metabolism ; Interleukin-6 - metabolism ; Interleukin-8 - metabolism ; Kinases ; Ligands ; Lipids ; Lipopolysaccharides ; Lipoteichoic acid ; Medicine and Health Sciences ; Mice ; Monocytes ; Monocytes - metabolism ; Monocytes - microbiology ; NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; Odontology ; Pathogenesis ; Pathogens ; Periodontal disease ; Periodontal Diseases - complications ; Periodontal Diseases - metabolism ; Periodontal Diseases - microbiology ; Periodontics ; Physical Sciences ; Plaque, Atherosclerotic - metabolism ; Plaque, Atherosclerotic - microbiology ; Plaques ; Porphyromonas gingivalis ; Porphyromonas gingivalis - metabolism ; Porphyromonas gingivalis - pathogenicity ; Proteins ; Rheumatology ; Signal transduction ; Staphylococcus aureus ; Staphylococcus aureus - chemistry ; Staphylococcus aureus - pathogenicity ; Stimulation ; Synergism ; Thyroid gland ; TLR2 protein ; TLR4 protein ; Toll-Like Receptor 2 - administration & dosage ; Toll-Like Receptor 2 - agonists ; Toll-Like Receptor 2 - metabolism ; Toll-Like Receptor 4 - administration & dosage ; Toll-Like Receptor 4 - agonists ; Toll-Like Receptor 4 - metabolism ; Toll-like receptors ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2017-02, Vol.12 (2), p.e0172773-e0172773</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Køllgaard et al. 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>2017 Køllgaard et al 2017 Køllgaard et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c791t-8f5582824d8392067599d7daa50c6674d02ef9f70137dd9fa704b6bad251ddb33</citedby><cites>FETCH-LOGICAL-c791t-8f5582824d8392067599d7daa50c6674d02ef9f70137dd9fa704b6bad251ddb33</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/PMC5325525/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5325525/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28235036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Amar, Salomon</contributor><creatorcontrib>Køllgaard, Tania</creatorcontrib><creatorcontrib>Enevold, Christian</creatorcontrib><creatorcontrib>Bendtzen, Klaus</creatorcontrib><creatorcontrib>Hansen, Peter R</creatorcontrib><creatorcontrib>Givskov, Michael</creatorcontrib><creatorcontrib>Holmstrup, Palle</creatorcontrib><creatorcontrib>Nielsen, Claus H</creatorcontrib><title>Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, including Porphyromonas gingivalis, have been found in atherosclerotic plaques in humans and mice. We aimed to determine whether cholesterol crystals (CHCs) and oral bacteria synergize in the stimulation of human monocytes. Incubation of human monocytes with CHCs induced secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-8. Moreover, CHCs markedly enhanced secretion of IL-1β by monocytes stimulated with the toll-like receptor (TLR) 4 agonist Escherichia coli lipopolysaccharide (LPS), and the TLR2 agonist Staphylococcus aureus lipoteichoic acid. Notably, CHCs also enhanced IL-1β secretion induced by P. gingivalis LPS and IL-1β secretion induced by whole P. gingivalis bacteria. This enhancement was abrogated by the NLRP3 inflammasome inhibitors Z-YVAD-FMK and glibenclamide. CHCs had no effect on cytokine production induced by P. gingivalis gingipains. Taken together, our findings support that CHCs, via stimulation of NLRP3 inflammasomes, act in synergy with the periodontal pathogen P. gingivalis to promote monocyte secretion of pro-atherogenic cytokines.</description><subject>Anaerobic bacteria</subject><subject>Animals</subject><subject>Arteriosclerosis</subject><subject>Atheroembolism</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - complications</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - microbiology</subject><subject>Bacteria</subject><subject>Biology and Life Sciences</subject><subject>Blood & organ donations</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cholesterol</subject><subject>Cholesterol - chemistry</subject><subject>Cholesterol - metabolism</subject><subject>Crystals</subject><subject>Cytokines</subject><subject>Dentistry</subject><subject>E coli</subject><subject>Epidemiology</subject><subject>Escherichia coli</subject><subject>Fibroblasts</subject><subject>Glibenclamide</subject><subject>Gram-positive bacteria</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immune system</subject><subject>Inflammasomes</subject><subject>Inflammasomes - drug effects</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Interleukin-8 - metabolism</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Lipids</subject><subject>Lipopolysaccharides</subject><subject>Lipoteichoic acid</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Monocytes</subject><subject>Monocytes - metabolism</subject><subject>Monocytes - microbiology</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>Odontology</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Periodontal disease</subject><subject>Periodontal Diseases - complications</subject><subject>Periodontal Diseases - metabolism</subject><subject>Periodontal Diseases - microbiology</subject><subject>Periodontics</subject><subject>Physical Sciences</subject><subject>Plaque, Atherosclerotic - metabolism</subject><subject>Plaque, Atherosclerotic - microbiology</subject><subject>Plaques</subject><subject>Porphyromonas gingivalis</subject><subject>Porphyromonas gingivalis - metabolism</subject><subject>Porphyromonas gingivalis - pathogenicity</subject><subject>Proteins</subject><subject>Rheumatology</subject><subject>Signal transduction</subject><subject>Staphylococcus aureus</subject><subject>Staphylococcus aureus - chemistry</subject><subject>Staphylococcus aureus - pathogenicity</subject><subject>Stimulation</subject><subject>Synergism</subject><subject>Thyroid gland</subject><subject>TLR2 protein</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 2 - administration & dosage</subject><subject>Toll-Like Receptor 2 - agonists</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-Like Receptor 4 - administration & dosage</subject><subject>Toll-Like Receptor 4 - agonists</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-like receptors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</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>2017</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>eNqNU01v1DAQjRCIlsI_QGAJCcEhi-3EcXJBqio-Kq1UVApXy7EniUtiL7ZTsb-HP4q33Va7qIcqBzv2e88zb2ay7CXBC1Jw8uHSzd7KcbFyFhaYcMp58Sg7JE1B84ri4vHO_iB7FsIlxqyoq-ppdkBrWjBcVIfZ35PBjRAieDci5dchyjEgsIO0CtDF8pzmSFq92ZX5BNrICBqtvMuN7UY5TTI6v0ZqHd0vYwF5CCmgAAG5Dk3OunSTfqJDcYANT6bVux6sUch5OaJWqvS6mSf0zfnVsPYu0WRAvbG9uZKjCc-zJ12KCl5s16Psx-dPFydf8-XZl9OT42WueENiXneM1SmzUtdFQ3HFWdNorqVkWFUVLzWm0DUdx8k-rZtOcly2VSs1ZUTrtiiOstc3uqvRBbH1NwhSc1LjAlOaEKc3CO3kpVh5M0m_Fk4acX3gfC-kj0aNIJqadJQwRTpoypaXspUNcICaQqta3CStj9vX5jYZq8DGZMee6P6NNYPo3ZVgBWWMsiTwbivg3e851VBMJigYR2nBzddx85ph0jwIShkvMduk-OY_6P1GbFG9TLmmVnApRLURFcdlTVmSutZa3INKn4bJqNS3nUnne4T3e4SEifAn9nIOQZx-P3849uznPvbtDnYAOcYhuHGOJvXqPrC8ASrvQvDQ3dWDYLEZu1s3xGbsxHbsEu3Vbi3vSLdzVvwDIW4q1A</recordid><startdate>20170224</startdate><enddate>20170224</enddate><creator>Køllgaard, Tania</creator><creator>Enevold, Christian</creator><creator>Bendtzen, Klaus</creator><creator>Hansen, Peter R</creator><creator>Givskov, Michael</creator><creator>Holmstrup, Palle</creator><creator>Nielsen, Claus H</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>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20170224</creationdate><title>Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis</title><author>Køllgaard, Tania ; Enevold, Christian ; Bendtzen, Klaus ; Hansen, Peter R ; Givskov, Michael ; Holmstrup, Palle ; Nielsen, Claus H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c791t-8f5582824d8392067599d7daa50c6674d02ef9f70137dd9fa704b6bad251ddb33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Anaerobic bacteria</topic><topic>Animals</topic><topic>Arteriosclerosis</topic><topic>Atheroembolism</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - complications</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - microbiology</topic><topic>Bacteria</topic><topic>Biology and Life Sciences</topic><topic>Blood & organ donations</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Cholesterol</topic><topic>Cholesterol - chemistry</topic><topic>Cholesterol - metabolism</topic><topic>Crystals</topic><topic>Cytokines</topic><topic>Dentistry</topic><topic>E coli</topic><topic>Epidemiology</topic><topic>Escherichia coli</topic><topic>Fibroblasts</topic><topic>Glibenclamide</topic><topic>Gram-positive bacteria</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immune system</topic><topic>Inflammasomes</topic><topic>Inflammasomes - drug effects</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-6 - metabolism</topic><topic>Interleukin-8 - metabolism</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Lipids</topic><topic>Lipopolysaccharides</topic><topic>Lipoteichoic acid</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Monocytes</topic><topic>Monocytes - metabolism</topic><topic>Monocytes - microbiology</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>Odontology</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Periodontal disease</topic><topic>Periodontal Diseases - complications</topic><topic>Periodontal Diseases - metabolism</topic><topic>Periodontal Diseases - microbiology</topic><topic>Periodontics</topic><topic>Physical Sciences</topic><topic>Plaque, Atherosclerotic - metabolism</topic><topic>Plaque, Atherosclerotic - microbiology</topic><topic>Plaques</topic><topic>Porphyromonas gingivalis</topic><topic>Porphyromonas gingivalis - metabolism</topic><topic>Porphyromonas gingivalis - pathogenicity</topic><topic>Proteins</topic><topic>Rheumatology</topic><topic>Signal transduction</topic><topic>Staphylococcus aureus</topic><topic>Staphylococcus aureus - chemistry</topic><topic>Staphylococcus aureus - pathogenicity</topic><topic>Stimulation</topic><topic>Synergism</topic><topic>Thyroid gland</topic><topic>TLR2 protein</topic><topic>TLR4 protein</topic><topic>Toll-Like Receptor 2 - administration & dosage</topic><topic>Toll-Like Receptor 2 - agonists</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-Like Receptor 4 - administration & dosage</topic><topic>Toll-Like Receptor 4 - agonists</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Toll-like receptors</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Køllgaard, Tania</creatorcontrib><creatorcontrib>Enevold, Christian</creatorcontrib><creatorcontrib>Bendtzen, Klaus</creatorcontrib><creatorcontrib>Hansen, Peter R</creatorcontrib><creatorcontrib>Givskov, Michael</creatorcontrib><creatorcontrib>Holmstrup, Palle</creatorcontrib><creatorcontrib>Nielsen, Claus H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</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>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</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>ProQuest Central China</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>Køllgaard, Tania</au><au>Enevold, Christian</au><au>Bendtzen, Klaus</au><au>Hansen, Peter R</au><au>Givskov, Michael</au><au>Holmstrup, Palle</au><au>Nielsen, Claus H</au><au>Amar, Salomon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-02-24</date><risdate>2017</risdate><volume>12</volume><issue>2</issue><spage>e0172773</spage><epage>e0172773</epage><pages>e0172773-e0172773</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, including Porphyromonas gingivalis, have been found in atherosclerotic plaques in humans and mice. We aimed to determine whether cholesterol crystals (CHCs) and oral bacteria synergize in the stimulation of human monocytes. Incubation of human monocytes with CHCs induced secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-8. Moreover, CHCs markedly enhanced secretion of IL-1β by monocytes stimulated with the toll-like receptor (TLR) 4 agonist Escherichia coli lipopolysaccharide (LPS), and the TLR2 agonist Staphylococcus aureus lipoteichoic acid. Notably, CHCs also enhanced IL-1β secretion induced by P. gingivalis LPS and IL-1β secretion induced by whole P. gingivalis bacteria. This enhancement was abrogated by the NLRP3 inflammasome inhibitors Z-YVAD-FMK and glibenclamide. CHCs had no effect on cytokine production induced by P. gingivalis gingipains. Taken together, our findings support that CHCs, via stimulation of NLRP3 inflammasomes, act in synergy with the periodontal pathogen P. gingivalis to promote monocyte secretion of pro-atherogenic cytokines.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28235036</pmid><doi>10.1371/journal.pone.0172773</doi><tpages>e0172773</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-02, Vol.12 (2), p.e0172773-e0172773 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1871803022 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Anaerobic bacteria Animals Arteriosclerosis Atheroembolism Atherosclerosis Atherosclerosis - complications Atherosclerosis - metabolism Atherosclerosis - microbiology Bacteria Biology and Life Sciences Blood & organ donations Cardiovascular disease Cardiovascular diseases Cholesterol Cholesterol - chemistry Cholesterol - metabolism Crystals Cytokines Dentistry E coli Epidemiology Escherichia coli Fibroblasts Glibenclamide Gram-positive bacteria Hospitals Humans Immune system Inflammasomes Inflammasomes - drug effects Inflammasomes - metabolism Inflammation Interleukin 6 Interleukin 8 Interleukin-1beta - metabolism Interleukin-6 - metabolism Interleukin-8 - metabolism Kinases Ligands Lipids Lipopolysaccharides Lipoteichoic acid Medicine and Health Sciences Mice Monocytes Monocytes - metabolism Monocytes - microbiology NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors NLR Family, Pyrin Domain-Containing 3 Protein - genetics Odontology Pathogenesis Pathogens Periodontal disease Periodontal Diseases - complications Periodontal Diseases - metabolism Periodontal Diseases - microbiology Periodontics Physical Sciences Plaque, Atherosclerotic - metabolism Plaque, Atherosclerotic - microbiology Plaques Porphyromonas gingivalis Porphyromonas gingivalis - metabolism Porphyromonas gingivalis - pathogenicity Proteins Rheumatology Signal transduction Staphylococcus aureus Staphylococcus aureus - chemistry Staphylococcus aureus - pathogenicity Stimulation Synergism Thyroid gland TLR2 protein TLR4 protein Toll-Like Receptor 2 - administration & dosage Toll-Like Receptor 2 - agonists Toll-Like Receptor 2 - metabolism Toll-Like Receptor 4 - administration & dosage Toll-Like Receptor 4 - agonists Toll-Like Receptor 4 - metabolism Toll-like receptors Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-19T06%3A02%3A53IST&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=Cholesterol%20crystals%20enhance%20TLR2-%20and%20TLR4-mediated%20pro-inflammatory%20cytokine%20responses%20of%20monocytes%20to%20the%20proatherogenic%20oral%20bacterium%20Porphyromonas%20gingivalis&rft.jtitle=PloS%20one&rft.au=K%C3%B8llgaard,%20Tania&rft.date=2017-02-24&rft.volume=12&rft.issue=2&rft.spage=e0172773&rft.epage=e0172773&rft.pages=e0172773-e0172773&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0172773&rft_dat=%3Cgale_plos_%3EA482540552%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=1871803022&rft_id=info:pmid/28235036&rft_galeid=A482540552&rft_doaj_id=oai_doaj_org_article_981f215c1fe94b74aba9e7ee82ebcb09&rfr_iscdi=true |