Elastin receptor (spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated human monocytes through NF-kappaB down-regulation

In inflammatory diseases, strong release of elastinolytic proteases results in elastin fiber degradation generating elastin peptides (EPs). Chemotactic activity for inflammatory cells was, among wide range of properties, the former identified biological activity exerted by EPs. Recently, we demonstr...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Journal of immunology (1950) 2007-11, Vol.179 (9), p.6184-6192
Hauptverfasser: Baranek, Thomas, Debret, Romain, Antonicelli, Frank, Lamkhioued, Bouchaib, Belaaouaj, Azzaq, Hornebeck, William, Bernard, Philippe, Guenounou, Moncef, Le Naour, Richard
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 6192
container_issue 9
container_start_page 6184
container_title The Journal of immunology (1950)
container_volume 179
creator Baranek, Thomas
Debret, Romain
Antonicelli, Frank
Lamkhioued, Bouchaib
Belaaouaj, Azzaq
Hornebeck, William
Bernard, Philippe
Guenounou, Moncef
Le Naour, Richard
description In inflammatory diseases, strong release of elastinolytic proteases results in elastin fiber degradation generating elastin peptides (EPs). Chemotactic activity for inflammatory cells was, among wide range of properties, the former identified biological activity exerted by EPs. Recently, we demonstrated the ability of EPs to favor a Th1 cytokine (IL-2, IFN-gamma) cell response in lymphocytes and to regulate IL-1beta expression in melanoma cells. We hypothesized that EPs might also influence inflammatory cell properties by regulating cytokine expression by these cells. Therefore, we investigated the influence of EPs on inflammatory cytokine synthesis by human monocytes. We evidenced that EPs down-regulated both at the mRNA and protein levels the proinflammatory TNF-alpha, IL-1beta, and IL-6 expression in LPS-activated monocytes. Such negative feedback loop could be accounted solely for EP-mediated effects on proinflammatory cytokine production because EPs did not affect anti-inflammatory IL-10 or TGF-beta secretion by LPS-activated monocytes. Furthermore, we demonstrated that EP effect on proinflammatory cytokine expression by LPS-stimulated monocytes could not be due either to a decrease of LPS receptor expression or to an alteration of LPS binding to its receptor. The inhibitory effects of EPs on cytokine expression were found to be mediated by receptor (spliced galactosidase) occupancy, as being suppressed by lactose, and to be associated with the decrease of NF-kappaB-DNA complex formation. As a whole, these results demonstrated that EP/spliced galactosidase interaction on human monocytes down-regulated NF-kappaB-dependent proinflammatory cytokine expression and pointed out the critical role of EPs in the regulation of inflammatory response.
format Article
fullrecord <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_00187289v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68408509</sourcerecordid><originalsourceid>FETCH-LOGICAL-h884-6cde9d58653c6931ebdff4dfd4a56b6ebddbc3aa03463bfde60aa9490964aa8c3</originalsourceid><addsrcrecordid>eNo9kcFu2zAMho2hw5ple4VCp6E9GJBjWbaOWdA0BYLtkrtBS3SsVpY0yV7nR9xbTUXTnQgS__cRID9kq6KqaM455VfZitLNJi9qXl9nn2N8opRyumGfsuuiFqzmgq2yv_cG4qQtCSjRTy6Q2-iNlqjIGQzIyUWtIOIdcVLOHqxcSLcQvFA-MVphJNLNdsKQgEh8cNr2BsYRknAhcpncs7ZI8I8PGKN2liTWaO-8M0sEKQcISZMn5zgbmNL2YR7BktFZl_C0YBqCm88D-bHPn8F7-E6Ue7F5wPMrkJRfso89mIhfL3Wdnfb3p90hP_58eNxtj_nQNCznUqFQVcOrUnJRFtipvmeqVwwq3vHUqk6WALRkvOx6hZwCCCao4AygkeU6u3vTDmBaH_QIYWkd6PawPbavM0qLpt404neRst_esukiv2aMUzvqKNEYsOjm2PKG0aaiIgVvLsG5G1H9977_qfwHqm2YNA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68408509</pqid></control><display><type>article</type><title>Elastin receptor (spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated human monocytes through NF-kappaB down-regulation</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Baranek, Thomas ; Debret, Romain ; Antonicelli, Frank ; Lamkhioued, Bouchaib ; Belaaouaj, Azzaq ; Hornebeck, William ; Bernard, Philippe ; Guenounou, Moncef ; Le Naour, Richard</creator><creatorcontrib>Baranek, Thomas ; Debret, Romain ; Antonicelli, Frank ; Lamkhioued, Bouchaib ; Belaaouaj, Azzaq ; Hornebeck, William ; Bernard, Philippe ; Guenounou, Moncef ; Le Naour, Richard</creatorcontrib><description>In inflammatory diseases, strong release of elastinolytic proteases results in elastin fiber degradation generating elastin peptides (EPs). Chemotactic activity for inflammatory cells was, among wide range of properties, the former identified biological activity exerted by EPs. Recently, we demonstrated the ability of EPs to favor a Th1 cytokine (IL-2, IFN-gamma) cell response in lymphocytes and to regulate IL-1beta expression in melanoma cells. We hypothesized that EPs might also influence inflammatory cell properties by regulating cytokine expression by these cells. Therefore, we investigated the influence of EPs on inflammatory cytokine synthesis by human monocytes. We evidenced that EPs down-regulated both at the mRNA and protein levels the proinflammatory TNF-alpha, IL-1beta, and IL-6 expression in LPS-activated monocytes. Such negative feedback loop could be accounted solely for EP-mediated effects on proinflammatory cytokine production because EPs did not affect anti-inflammatory IL-10 or TGF-beta secretion by LPS-activated monocytes. Furthermore, we demonstrated that EP effect on proinflammatory cytokine expression by LPS-stimulated monocytes could not be due either to a decrease of LPS receptor expression or to an alteration of LPS binding to its receptor. The inhibitory effects of EPs on cytokine expression were found to be mediated by receptor (spliced galactosidase) occupancy, as being suppressed by lactose, and to be associated with the decrease of NF-kappaB-DNA complex formation. As a whole, these results demonstrated that EP/spliced galactosidase interaction on human monocytes down-regulated NF-kappaB-dependent proinflammatory cytokine expression and pointed out the critical role of EPs in the regulation of inflammatory response.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>PMID: 17947694</identifier><language>eng</language><publisher>United States: Publisher : Baltimore : Williams &amp; Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists</publisher><subject>Cells, Cultured ; Cytokines - biosynthesis ; DNA - metabolism ; Down-Regulation - drug effects ; Elastin - metabolism ; Humans ; Lipopolysaccharide Receptors - metabolism ; Lipopolysaccharides - pharmacology ; Melanoma - genetics ; Melanoma - metabolism ; Monocytes - drug effects ; Monocytes - metabolism ; NF-kappa B - metabolism ; Peptide Fragments - metabolism ; Protein Binding ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; Signal Transduction ; Toll-Like Receptor 4 - metabolism</subject><ispartof>The Journal of immunology (1950), 2007-11, Vol.179 (9), p.6184-6192</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-6315-2616</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17947694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00187289$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Baranek, Thomas</creatorcontrib><creatorcontrib>Debret, Romain</creatorcontrib><creatorcontrib>Antonicelli, Frank</creatorcontrib><creatorcontrib>Lamkhioued, Bouchaib</creatorcontrib><creatorcontrib>Belaaouaj, Azzaq</creatorcontrib><creatorcontrib>Hornebeck, William</creatorcontrib><creatorcontrib>Bernard, Philippe</creatorcontrib><creatorcontrib>Guenounou, Moncef</creatorcontrib><creatorcontrib>Le Naour, Richard</creatorcontrib><title>Elastin receptor (spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated human monocytes through NF-kappaB down-regulation</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>In inflammatory diseases, strong release of elastinolytic proteases results in elastin fiber degradation generating elastin peptides (EPs). Chemotactic activity for inflammatory cells was, among wide range of properties, the former identified biological activity exerted by EPs. Recently, we demonstrated the ability of EPs to favor a Th1 cytokine (IL-2, IFN-gamma) cell response in lymphocytes and to regulate IL-1beta expression in melanoma cells. We hypothesized that EPs might also influence inflammatory cell properties by regulating cytokine expression by these cells. Therefore, we investigated the influence of EPs on inflammatory cytokine synthesis by human monocytes. We evidenced that EPs down-regulated both at the mRNA and protein levels the proinflammatory TNF-alpha, IL-1beta, and IL-6 expression in LPS-activated monocytes. Such negative feedback loop could be accounted solely for EP-mediated effects on proinflammatory cytokine production because EPs did not affect anti-inflammatory IL-10 or TGF-beta secretion by LPS-activated monocytes. Furthermore, we demonstrated that EP effect on proinflammatory cytokine expression by LPS-stimulated monocytes could not be due either to a decrease of LPS receptor expression or to an alteration of LPS binding to its receptor. The inhibitory effects of EPs on cytokine expression were found to be mediated by receptor (spliced galactosidase) occupancy, as being suppressed by lactose, and to be associated with the decrease of NF-kappaB-DNA complex formation. As a whole, these results demonstrated that EP/spliced galactosidase interaction on human monocytes down-regulated NF-kappaB-dependent proinflammatory cytokine expression and pointed out the critical role of EPs in the regulation of inflammatory response.</description><subject>Cells, Cultured</subject><subject>Cytokines - biosynthesis</subject><subject>DNA - metabolism</subject><subject>Down-Regulation - drug effects</subject><subject>Elastin - metabolism</subject><subject>Humans</subject><subject>Lipopolysaccharide Receptors - metabolism</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Monocytes - drug effects</subject><subject>Monocytes - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Peptide Fragments - metabolism</subject><subject>Protein Binding</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Signal Transduction</subject><subject>Toll-Like Receptor 4 - metabolism</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kcFu2zAMho2hw5ple4VCp6E9GJBjWbaOWdA0BYLtkrtBS3SsVpY0yV7nR9xbTUXTnQgS__cRID9kq6KqaM455VfZitLNJi9qXl9nn2N8opRyumGfsuuiFqzmgq2yv_cG4qQtCSjRTy6Q2-iNlqjIGQzIyUWtIOIdcVLOHqxcSLcQvFA-MVphJNLNdsKQgEh8cNr2BsYRknAhcpncs7ZI8I8PGKN2liTWaO-8M0sEKQcISZMn5zgbmNL2YR7BktFZl_C0YBqCm88D-bHPn8F7-E6Ue7F5wPMrkJRfso89mIhfL3Wdnfb3p90hP_58eNxtj_nQNCznUqFQVcOrUnJRFtipvmeqVwwq3vHUqk6WALRkvOx6hZwCCCao4AygkeU6u3vTDmBaH_QIYWkd6PawPbavM0qLpt404neRst_esukiv2aMUzvqKNEYsOjm2PKG0aaiIgVvLsG5G1H9977_qfwHqm2YNA</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>Baranek, Thomas</creator><creator>Debret, Romain</creator><creator>Antonicelli, Frank</creator><creator>Lamkhioued, Bouchaib</creator><creator>Belaaouaj, Azzaq</creator><creator>Hornebeck, William</creator><creator>Bernard, Philippe</creator><creator>Guenounou, Moncef</creator><creator>Le Naour, Richard</creator><general>Publisher : Baltimore : Williams &amp; Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-6315-2616</orcidid></search><sort><creationdate>20071101</creationdate><title>Elastin receptor (spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated human monocytes through NF-kappaB down-regulation</title><author>Baranek, Thomas ; Debret, Romain ; Antonicelli, Frank ; Lamkhioued, Bouchaib ; Belaaouaj, Azzaq ; Hornebeck, William ; Bernard, Philippe ; Guenounou, Moncef ; Le Naour, Richard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h884-6cde9d58653c6931ebdff4dfd4a56b6ebddbc3aa03463bfde60aa9490964aa8c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Cells, Cultured</topic><topic>Cytokines - biosynthesis</topic><topic>DNA - metabolism</topic><topic>Down-Regulation - drug effects</topic><topic>Elastin - metabolism</topic><topic>Humans</topic><topic>Lipopolysaccharide Receptors - metabolism</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Melanoma - genetics</topic><topic>Melanoma - metabolism</topic><topic>Monocytes - drug effects</topic><topic>Monocytes - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Peptide Fragments - metabolism</topic><topic>Protein Binding</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Signal Transduction</topic><topic>Toll-Like Receptor 4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baranek, Thomas</creatorcontrib><creatorcontrib>Debret, Romain</creatorcontrib><creatorcontrib>Antonicelli, Frank</creatorcontrib><creatorcontrib>Lamkhioued, Bouchaib</creatorcontrib><creatorcontrib>Belaaouaj, Azzaq</creatorcontrib><creatorcontrib>Hornebeck, William</creatorcontrib><creatorcontrib>Bernard, Philippe</creatorcontrib><creatorcontrib>Guenounou, Moncef</creatorcontrib><creatorcontrib>Le Naour, Richard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baranek, Thomas</au><au>Debret, Romain</au><au>Antonicelli, Frank</au><au>Lamkhioued, Bouchaib</au><au>Belaaouaj, Azzaq</au><au>Hornebeck, William</au><au>Bernard, Philippe</au><au>Guenounou, Moncef</au><au>Le Naour, Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Elastin receptor (spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated human monocytes through NF-kappaB down-regulation</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>179</volume><issue>9</issue><spage>6184</spage><epage>6192</epage><pages>6184-6192</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>In inflammatory diseases, strong release of elastinolytic proteases results in elastin fiber degradation generating elastin peptides (EPs). Chemotactic activity for inflammatory cells was, among wide range of properties, the former identified biological activity exerted by EPs. Recently, we demonstrated the ability of EPs to favor a Th1 cytokine (IL-2, IFN-gamma) cell response in lymphocytes and to regulate IL-1beta expression in melanoma cells. We hypothesized that EPs might also influence inflammatory cell properties by regulating cytokine expression by these cells. Therefore, we investigated the influence of EPs on inflammatory cytokine synthesis by human monocytes. We evidenced that EPs down-regulated both at the mRNA and protein levels the proinflammatory TNF-alpha, IL-1beta, and IL-6 expression in LPS-activated monocytes. Such negative feedback loop could be accounted solely for EP-mediated effects on proinflammatory cytokine production because EPs did not affect anti-inflammatory IL-10 or TGF-beta secretion by LPS-activated monocytes. Furthermore, we demonstrated that EP effect on proinflammatory cytokine expression by LPS-stimulated monocytes could not be due either to a decrease of LPS receptor expression or to an alteration of LPS binding to its receptor. The inhibitory effects of EPs on cytokine expression were found to be mediated by receptor (spliced galactosidase) occupancy, as being suppressed by lactose, and to be associated with the decrease of NF-kappaB-DNA complex formation. As a whole, these results demonstrated that EP/spliced galactosidase interaction on human monocytes down-regulated NF-kappaB-dependent proinflammatory cytokine expression and pointed out the critical role of EPs in the regulation of inflammatory response.</abstract><cop>United States</cop><pub>Publisher : Baltimore : Williams &amp; Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists</pub><pmid>17947694</pmid><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-6315-2616</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0022-1767
ispartof The Journal of immunology (1950), 2007-11, Vol.179 (9), p.6184-6192
issn 0022-1767
1550-6606
language eng
recordid cdi_hal_primary_oai_HAL_hal_00187289v1
source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Cells, Cultured
Cytokines - biosynthesis
DNA - metabolism
Down-Regulation - drug effects
Elastin - metabolism
Humans
Lipopolysaccharide Receptors - metabolism
Lipopolysaccharides - pharmacology
Melanoma - genetics
Melanoma - metabolism
Monocytes - drug effects
Monocytes - metabolism
NF-kappa B - metabolism
Peptide Fragments - metabolism
Protein Binding
Protein Isoforms - genetics
Protein Isoforms - metabolism
Receptors, Cell Surface - genetics
Receptors, Cell Surface - metabolism
Signal Transduction
Toll-Like Receptor 4 - metabolism
title Elastin receptor (spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated human monocytes through NF-kappaB down-regulation
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T03%3A08%3A53IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_hal_p&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Elastin%20receptor%20(spliced%20galactosidase)%20occupancy%20by%20elastin%20peptides%20counteracts%20proinflammatory%20cytokine%20expression%20in%20lipopolysaccharide-stimulated%20human%20monocytes%20through%20NF-kappaB%20down-regulation&rft.jtitle=The%20Journal%20of%20immunology%20(1950)&rft.au=Baranek,%20Thomas&rft.date=2007-11-01&rft.volume=179&rft.issue=9&rft.spage=6184&rft.epage=6192&rft.pages=6184-6192&rft.issn=0022-1767&rft.eissn=1550-6606&rft_id=info:doi/&rft_dat=%3Cproquest_hal_p%3E68408509%3C/proquest_hal_p%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=68408509&rft_id=info:pmid/17947694&rfr_iscdi=true