Effects of Endocrine Disruptor Compounds, Alone or in Combination, on Human Macrophage-Like THP-1 Cell Response
The aim of the present study was to evaluate the immunological effects on human macrophages of four endocrine disruptor compounds (EDCs) using the differentiated human THP-1 cell line as a model. We studied first the effects of these EDCs, including Bisphenol A (BPA), di-ethylhexyl-phthalate (DEHP),...
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| Veröffentlicht in: | PloS one 2015-07, Vol.10 (7), p.e0131428-e0131428 |
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| creator | Couleau, N Falla, J Beillerot, A Battaglia, E D'Innocenzo, M Plançon, S Laval-Gilly, P Bennasroune, A |
| description | The aim of the present study was to evaluate the immunological effects on human macrophages of four endocrine disruptor compounds (EDCs) using the differentiated human THP-1 cell line as a model. We studied first the effects of these EDCs, including Bisphenol A (BPA), di-ethylhexyl-phthalate (DEHP), dibutyl phthalate (DBP) and 4-tert-octylphenol (4-OP), either alone or in combination, on cytokine secretion, and phagocytosis. We then determined whether or not these effects were mediated by estrogen receptors via MAPK pathways. It was found that all four EDCs studied reduced strongly the phagocytosis of the differentiated THP-1 cells and that several of these EDCs disturbed also TNF-α, IL-1 β and IL-8 cytokine secretions. Furthermore, relative to control treatment, decreased ERK 1/2 phosphorylation was always associated with EDCs treatments-either alone or in certain combinations (at 0.1 μM for each condition). Lastly, as treatments by an estrogen receptor antagonist suppressed the negative effects on ERK 1/2 phosphorylation observed in cells treated either alone with BPA, DEHP, 4-OP or with the combined treatment of BPA and DEHP, we suggested that estrogen receptor-dependent pathway is involved in mediating the effects of EDCs on human immune system. Altogether, these results advocate that EDCs can disturb human immune response at very low concentrations. |
| doi_str_mv | 10.1371/journal.pone.0131428 |
| format | Article |
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We studied first the effects of these EDCs, including Bisphenol A (BPA), di-ethylhexyl-phthalate (DEHP), dibutyl phthalate (DBP) and 4-tert-octylphenol (4-OP), either alone or in combination, on cytokine secretion, and phagocytosis. We then determined whether or not these effects were mediated by estrogen receptors via MAPK pathways. It was found that all four EDCs studied reduced strongly the phagocytosis of the differentiated THP-1 cells and that several of these EDCs disturbed also TNF-α, IL-1 β and IL-8 cytokine secretions. Furthermore, relative to control treatment, decreased ERK 1/2 phosphorylation was always associated with EDCs treatments-either alone or in certain combinations (at 0.1 μM for each condition). Lastly, as treatments by an estrogen receptor antagonist suppressed the negative effects on ERK 1/2 phosphorylation observed in cells treated either alone with BPA, DEHP, 4-OP or with the combined treatment of BPA and DEHP, we suggested that estrogen receptor-dependent pathway is involved in mediating the effects of EDCs on human immune system. Altogether, these results advocate that EDCs can disturb human immune response at very low concentrations.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0131428</identifier><identifier>PMID: 26133781</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>4-tert-Octylphenol ; Benzhydryl Compounds - pharmacology ; Bisphenol A ; Cell Line ; Combined treatment ; Cytokines ; Dibutyl phthalate ; Dibutyl Phthalate - pharmacology ; Diethylhexyl Phthalate - pharmacology ; Dioctyl phthalate ; Dose-Response Relationship, Drug ; Endocrine disruptors ; Endocrine Disruptors - pharmacology ; Estrogen receptors ; Estrogens ; Gene Expression Regulation ; Human behavior ; Humans ; Immune response ; Immune system ; Immunology ; Interleukin 1 ; Interleukin 8 ; Interleukin-1beta - agonists ; Interleukin-1beta - metabolism ; Interleukin-8 - agonists ; Interleukin-8 - metabolism ; Kinases ; Life Sciences ; Low concentrations ; Macrophages ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - metabolism ; MAP kinase ; Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors ; Mitogen-Activated Protein Kinase 1 - genetics ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors ; Mitogen-Activated Protein Kinase 3 - genetics ; Mitogen-Activated Protein Kinase 3 - metabolism ; Pesticides ; Phagocytosis ; Phagocytosis - drug effects ; Phenols ; Phenols - pharmacology ; Phosphorylation ; Phosphorylation - drug effects ; Receptors ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Secretions ; Signal Transduction ; Toxicology ; Tumor Necrosis Factor-alpha - agonists ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α ; Zebrafish</subject><ispartof>PloS one, 2015-07, Vol.10 (7), p.e0131428-e0131428</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Couleau 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>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>2015 Couleau et al 2015 Couleau et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c726t-11ce846bde143f8a1fbb3a6a7ed77edeec9d3489f5befc4212d1120b6a8646b63</citedby><cites>FETCH-LOGICAL-c726t-11ce846bde143f8a1fbb3a6a7ed77edeec9d3489f5befc4212d1120b6a8646b63</cites><orcidid>0000-0003-3162-3043</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4489735/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4489735/$$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/26133781$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01248831$$DView record in HAL$$Hfree_for_read</backlink></links><search><contributor>Rosenfeld, Cheryl S.</contributor><creatorcontrib>Couleau, N</creatorcontrib><creatorcontrib>Falla, J</creatorcontrib><creatorcontrib>Beillerot, A</creatorcontrib><creatorcontrib>Battaglia, E</creatorcontrib><creatorcontrib>D'Innocenzo, M</creatorcontrib><creatorcontrib>Plançon, S</creatorcontrib><creatorcontrib>Laval-Gilly, P</creatorcontrib><creatorcontrib>Bennasroune, A</creatorcontrib><title>Effects of Endocrine Disruptor Compounds, Alone or in Combination, on Human Macrophage-Like THP-1 Cell Response</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The aim of the present study was to evaluate the immunological effects on human macrophages of four endocrine disruptor compounds (EDCs) using the differentiated human THP-1 cell line as a model. We studied first the effects of these EDCs, including Bisphenol A (BPA), di-ethylhexyl-phthalate (DEHP), dibutyl phthalate (DBP) and 4-tert-octylphenol (4-OP), either alone or in combination, on cytokine secretion, and phagocytosis. We then determined whether or not these effects were mediated by estrogen receptors via MAPK pathways. It was found that all four EDCs studied reduced strongly the phagocytosis of the differentiated THP-1 cells and that several of these EDCs disturbed also TNF-α, IL-1 β and IL-8 cytokine secretions. Furthermore, relative to control treatment, decreased ERK 1/2 phosphorylation was always associated with EDCs treatments-either alone or in certain combinations (at 0.1 μM for each condition). Lastly, as treatments by an estrogen receptor antagonist suppressed the negative effects on ERK 1/2 phosphorylation observed in cells treated either alone with BPA, DEHP, 4-OP or with the combined treatment of BPA and DEHP, we suggested that estrogen receptor-dependent pathway is involved in mediating the effects of EDCs on human immune system. Altogether, these results advocate that EDCs can disturb human immune response at very low concentrations.</description><subject>4-tert-Octylphenol</subject><subject>Benzhydryl Compounds - pharmacology</subject><subject>Bisphenol A</subject><subject>Cell Line</subject><subject>Combined treatment</subject><subject>Cytokines</subject><subject>Dibutyl phthalate</subject><subject>Dibutyl Phthalate - pharmacology</subject><subject>Diethylhexyl Phthalate - pharmacology</subject><subject>Dioctyl phthalate</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endocrine disruptors</subject><subject>Endocrine Disruptors - pharmacology</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Gene Expression Regulation</subject><subject>Human behavior</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Interleukin 1</subject><subject>Interleukin 8</subject><subject>Interleukin-1beta - 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pharmacology</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Receptors</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Secretions</subject><subject>Signal Transduction</subject><subject>Toxicology</subject><subject>Tumor Necrosis Factor-alpha - agonists</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>Zebrafish</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>eNqNk29v0zAQxiMEYqPwDRBEmoSYtJT4T53kDVJVCq1UNDQGby0nPrcuiR3iZIJvj7NmUzPtBYqiWJffPWc_vguC1yieIpKgD3vbNUaU09oamMaIIIrTJ8EpygiOGI7J06P1SfDCuX0cz0jK2PPgBDNESJKi08AulYKidaFV4dJIWzTaQPhJu6arW9uEC1vVtjPSXYTz0lcKfUybPpxrI1ptzUVoTbjqKmHCr6JobL0TW4g2-heE16tvEQoXUJbhFTi_UQcvg2dKlA5eDd9J8OPz8nqxijaXX9aL-SYqEszaCKECUspyCYgSlQqk8pwIJhKQiX8BikwSmmZqloMqKEZYIoTjnImU-TRGJsHbg25dWscHrxxHLCMozbyBnlgfCGnFnteNrkTzl1uh-W3ANlsumlYXJXBFQSDBGEUspRJklsVJnmBFpJJ4lkuv9XGo1uUVyAJM24hyJDr-Y_SOb-0Np_4MCZl5gfODwO5B2mq-4X0sRpimKUE3yLPvh2KN_d2Ba3mlXeFNFgZsd3tGmjF_w9ijZw_Qx50YqK3wh9VGWb_Hohflc4pjnCbEw5Ng-gjlHwmVLnxrKO3jo4TzUYJnWvjTbkXnHF9_v_p_9vLnmH13xO5AlO3O2bLrm9GNQXoAfVc614C6dxbFvJ-hOzd4P0N8mCGf9ub4Mu-T7oaG_AOobxWV</recordid><startdate>20150702</startdate><enddate>20150702</enddate><creator>Couleau, N</creator><creator>Falla, J</creator><creator>Beillerot, A</creator><creator>Battaglia, E</creator><creator>D'Innocenzo, M</creator><creator>Plançon, S</creator><creator>Laval-Gilly, P</creator><creator>Bennasroune, A</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>1XC</scope><scope>VOOES</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-3162-3043</orcidid></search><sort><creationdate>20150702</creationdate><title>Effects of Endocrine Disruptor Compounds, Alone or in Combination, on Human Macrophage-Like THP-1 Cell Response</title><author>Couleau, N ; Falla, J ; Beillerot, A ; Battaglia, E ; D'Innocenzo, M ; Plançon, S ; Laval-Gilly, P ; Bennasroune, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c726t-11ce846bde143f8a1fbb3a6a7ed77edeec9d3489f5befc4212d1120b6a8646b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>4-tert-Octylphenol</topic><topic>Benzhydryl Compounds - pharmacology</topic><topic>Bisphenol A</topic><topic>Cell Line</topic><topic>Combined treatment</topic><topic>Cytokines</topic><topic>Dibutyl phthalate</topic><topic>Dibutyl Phthalate - pharmacology</topic><topic>Diethylhexyl Phthalate - pharmacology</topic><topic>Dioctyl phthalate</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endocrine disruptors</topic><topic>Endocrine Disruptors - pharmacology</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Gene Expression Regulation</topic><topic>Human behavior</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Interleukin 1</topic><topic>Interleukin 8</topic><topic>Interleukin-1beta - agonists</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-8 - agonists</topic><topic>Interleukin-8 - metabolism</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Low concentrations</topic><topic>Macrophages</topic><topic>Macrophages - 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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>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</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>Couleau, N</au><au>Falla, J</au><au>Beillerot, A</au><au>Battaglia, E</au><au>D'Innocenzo, M</au><au>Plançon, S</au><au>Laval-Gilly, P</au><au>Bennasroune, A</au><au>Rosenfeld, Cheryl S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Endocrine Disruptor Compounds, Alone or in Combination, on Human Macrophage-Like THP-1 Cell Response</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-07-02</date><risdate>2015</risdate><volume>10</volume><issue>7</issue><spage>e0131428</spage><epage>e0131428</epage><pages>e0131428-e0131428</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The aim of the present study was to evaluate the immunological effects on human macrophages of four endocrine disruptor compounds (EDCs) using the differentiated human THP-1 cell line as a model. We studied first the effects of these EDCs, including Bisphenol A (BPA), di-ethylhexyl-phthalate (DEHP), dibutyl phthalate (DBP) and 4-tert-octylphenol (4-OP), either alone or in combination, on cytokine secretion, and phagocytosis. We then determined whether or not these effects were mediated by estrogen receptors via MAPK pathways. It was found that all four EDCs studied reduced strongly the phagocytosis of the differentiated THP-1 cells and that several of these EDCs disturbed also TNF-α, IL-1 β and IL-8 cytokine secretions. Furthermore, relative to control treatment, decreased ERK 1/2 phosphorylation was always associated with EDCs treatments-either alone or in certain combinations (at 0.1 μM for each condition). Lastly, as treatments by an estrogen receptor antagonist suppressed the negative effects on ERK 1/2 phosphorylation observed in cells treated either alone with BPA, DEHP, 4-OP or with the combined treatment of BPA and DEHP, we suggested that estrogen receptor-dependent pathway is involved in mediating the effects of EDCs on human immune system. Altogether, these results advocate that EDCs can disturb human immune response at very low concentrations.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26133781</pmid><doi>10.1371/journal.pone.0131428</doi><orcidid>https://orcid.org/0000-0003-3162-3043</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-07, Vol.10 (7), p.e0131428-e0131428 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1693189137 |
| 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 | 4-tert-Octylphenol Benzhydryl Compounds - pharmacology Bisphenol A Cell Line Combined treatment Cytokines Dibutyl phthalate Dibutyl Phthalate - pharmacology Diethylhexyl Phthalate - pharmacology Dioctyl phthalate Dose-Response Relationship, Drug Endocrine disruptors Endocrine Disruptors - pharmacology Estrogen receptors Estrogens Gene Expression Regulation Human behavior Humans Immune response Immune system Immunology Interleukin 1 Interleukin 8 Interleukin-1beta - agonists Interleukin-1beta - metabolism Interleukin-8 - agonists Interleukin-8 - metabolism Kinases Life Sciences Low concentrations Macrophages Macrophages - cytology Macrophages - drug effects Macrophages - metabolism MAP kinase Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors Mitogen-Activated Protein Kinase 1 - genetics Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors Mitogen-Activated Protein Kinase 3 - genetics Mitogen-Activated Protein Kinase 3 - metabolism Pesticides Phagocytosis Phagocytosis - drug effects Phenols Phenols - pharmacology Phosphorylation Phosphorylation - drug effects Receptors Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Secretions Signal Transduction Toxicology Tumor Necrosis Factor-alpha - agonists Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α Zebrafish |
| title | Effects of Endocrine Disruptor Compounds, Alone or in Combination, on Human Macrophage-Like THP-1 Cell Response |
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