The impact of the level and distribution of methyl-esters of pectins on TLR2-1 dependent anti-inflammatory responses
•Homogalacturonan pectins mainly inhibit TLR2-1.•Pectins with a low DM or intermediate DM with a high DB inhibited TLR2-1 strongest.•TLR2 bound strongest to pectins with a low DM or an intermediate DM with a high DB.•TLR2-1 inhibiting pectins also inhibited IL-6 secretion from macrophages. Pectins h...
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| Veröffentlicht in: | Carbohydrate polymers 2021-01, Vol.251, p.117093-117093, Article 117093 |
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| container_title | Carbohydrate polymers |
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| creator | Beukema, M. Jermendi, É. van den Berg, M.A. Faas, M.M. Schols, H.A. de Vos, P. |
| description | •Homogalacturonan pectins mainly inhibit TLR2-1.•Pectins with a low DM or intermediate DM with a high DB inhibited TLR2-1 strongest.•TLR2 bound strongest to pectins with a low DM or an intermediate DM with a high DB.•TLR2-1 inhibiting pectins also inhibited IL-6 secretion from macrophages.
Pectins have anti-inflammatory effects via Toll-like receptor (TLR) inhibition in a degree of methyl-esterification-(DM)-dependent manner. However, pectins also vary in distribution of methyl-esters over the galacturonic-acid (GalA) backbone (Degree of Blockiness - DB) and impact of this on anti-inflammatory capacity is unknown. Pectins mainly inhibit TLR2-1 but magnitude depends on both DM and DB. Low DM pectins (DM18/19) with both low (DB86) and high DB (DB94) strongly inhibit TLR2-1. However, pectins with intermediate DM (DM43/DM49) and high DB (DB60), but not with low DB (DB33), inhibit TLR2-1 as strongly as low DM. High DM pectins (DM84/88) with DB71 and DB91 do not inhibit TLR2-1 strongly. Pectin-binding to TLR2 was confirmed by capture-ELISA. In human macrophages, low DM and intermediate DM pectins with high DB inhibited TLR2-1 induced IL-6 secretion. Both high number and blockwise distribution of non-esterified GalA in pectins are responsible for the anti-inflammatory effects via inhibition of TLR2-1. |
| doi_str_mv | 10.1016/j.carbpol.2020.117093 |
| format | Article |
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Pectins have anti-inflammatory effects via Toll-like receptor (TLR) inhibition in a degree of methyl-esterification-(DM)-dependent manner. However, pectins also vary in distribution of methyl-esters over the galacturonic-acid (GalA) backbone (Degree of Blockiness - DB) and impact of this on anti-inflammatory capacity is unknown. Pectins mainly inhibit TLR2-1 but magnitude depends on both DM and DB. Low DM pectins (DM18/19) with both low (DB86) and high DB (DB94) strongly inhibit TLR2-1. However, pectins with intermediate DM (DM43/DM49) and high DB (DB60), but not with low DB (DB33), inhibit TLR2-1 as strongly as low DM. High DM pectins (DM84/88) with DB71 and DB91 do not inhibit TLR2-1 strongly. Pectin-binding to TLR2 was confirmed by capture-ELISA. In human macrophages, low DM and intermediate DM pectins with high DB inhibited TLR2-1 induced IL-6 secretion. Both high number and blockwise distribution of non-esterified GalA in pectins are responsible for the anti-inflammatory effects via inhibition of TLR2-1.</description><identifier>ISSN: 0144-8617</identifier><identifier>EISSN: 1879-1344</identifier><identifier>DOI: 10.1016/j.carbpol.2020.117093</identifier><identifier>PMID: 33152851</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Anti-Inflammatory Agents - chemistry ; Anti-Inflammatory Agents - pharmacology ; Cell Line ; Chromatography, High Pressure Liquid ; Degree of blockiness ; Degree of methyl-esterification ; Esterification ; Esters - chemistry ; Esters - metabolism ; Hexuronic Acids - chemistry ; Humans ; Inflammation - metabolism ; Macrophages ; Pectin ; Pectins - chemistry ; Pectins - pharmacology ; Toll-like receptor 2 ; Toll-Like Receptor 2 - drug effects ; Toll-Like Receptor 2 - metabolism</subject><ispartof>Carbohydrate polymers, 2021-01, Vol.251, p.117093-117093, Article 117093</ispartof><rights>2020 The Authors</rights><rights>Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-50d3e7a10d19996d0dbea321700ad83d7c000ee1255c966e338863b684fdcd673</citedby><cites>FETCH-LOGICAL-c478t-50d3e7a10d19996d0dbea321700ad83d7c000ee1255c966e338863b684fdcd673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.carbpol.2020.117093$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33152851$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Beukema, M.</creatorcontrib><creatorcontrib>Jermendi, É.</creatorcontrib><creatorcontrib>van den Berg, M.A.</creatorcontrib><creatorcontrib>Faas, M.M.</creatorcontrib><creatorcontrib>Schols, H.A.</creatorcontrib><creatorcontrib>de Vos, P.</creatorcontrib><title>The impact of the level and distribution of methyl-esters of pectins on TLR2-1 dependent anti-inflammatory responses</title><title>Carbohydrate polymers</title><addtitle>Carbohydr Polym</addtitle><description>•Homogalacturonan pectins mainly inhibit TLR2-1.•Pectins with a low DM or intermediate DM with a high DB inhibited TLR2-1 strongest.•TLR2 bound strongest to pectins with a low DM or an intermediate DM with a high DB.•TLR2-1 inhibiting pectins also inhibited IL-6 secretion from macrophages.
Pectins have anti-inflammatory effects via Toll-like receptor (TLR) inhibition in a degree of methyl-esterification-(DM)-dependent manner. However, pectins also vary in distribution of methyl-esters over the galacturonic-acid (GalA) backbone (Degree of Blockiness - DB) and impact of this on anti-inflammatory capacity is unknown. Pectins mainly inhibit TLR2-1 but magnitude depends on both DM and DB. Low DM pectins (DM18/19) with both low (DB86) and high DB (DB94) strongly inhibit TLR2-1. However, pectins with intermediate DM (DM43/DM49) and high DB (DB60), but not with low DB (DB33), inhibit TLR2-1 as strongly as low DM. High DM pectins (DM84/88) with DB71 and DB91 do not inhibit TLR2-1 strongly. Pectin-binding to TLR2 was confirmed by capture-ELISA. In human macrophages, low DM and intermediate DM pectins with high DB inhibited TLR2-1 induced IL-6 secretion. Both high number and blockwise distribution of non-esterified GalA in pectins are responsible for the anti-inflammatory effects via inhibition of TLR2-1.</description><subject>Anti-Inflammatory Agents - chemistry</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Cell Line</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Degree of blockiness</subject><subject>Degree of methyl-esterification</subject><subject>Esterification</subject><subject>Esters - chemistry</subject><subject>Esters - metabolism</subject><subject>Hexuronic Acids - chemistry</subject><subject>Humans</subject><subject>Inflammation - metabolism</subject><subject>Macrophages</subject><subject>Pectin</subject><subject>Pectins - chemistry</subject><subject>Pectins - pharmacology</subject><subject>Toll-like receptor 2</subject><subject>Toll-Like Receptor 2 - drug effects</subject><subject>Toll-Like Receptor 2 - metabolism</subject><issn>0144-8617</issn><issn>1879-1344</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1PxCAQhonR6Lr6EzQ9eukKpQV6Msb4lWxiYtYzoTCNbFqowJrsv5fNrl7lMjDzzgzvg9AVwQuCCbtdL7QK3eSHRYWrnCMct_QIzYjgbUloXR-jGSZ1XQpG-Bk6j3GN82EEn6IzSklTiYbMUFp9QmHHSelU-L5I-TXANwyFcqYwNqZgu02y3u2qI6TP7VBCTBDiLjGBTtblqytWy_eqJIWBCZwBl_KAZEvr-kGNo0o-bIsAcfIuQrxAJ70aIlwe4hx9PD2uHl7K5dvz68P9stQ1F6lssKHAFcGGtG3LDDYdKFplp1gZQQ3X2RAAqZpGt4wBpUIw2jFR90Ybxukc3eznTsF_bfK35WijhmFQDvwmyqpuBKa84ixLm71UBx9jgF5OwY4qbCXBcgdcruUBuNwBl3vgue_6sGLTjWD-un4JZ8HdXgDZ6LeFIKO24DQYGzI9abz9Z8UPLDWUqw</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Beukema, M.</creator><creator>Jermendi, É.</creator><creator>van den Berg, M.A.</creator><creator>Faas, M.M.</creator><creator>Schols, H.A.</creator><creator>de Vos, P.</creator><general>Elsevier Ltd</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>20210101</creationdate><title>The impact of the level and distribution of methyl-esters of pectins on TLR2-1 dependent anti-inflammatory responses</title><author>Beukema, M. ; Jermendi, É. ; van den Berg, M.A. ; Faas, M.M. ; Schols, H.A. ; de Vos, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-50d3e7a10d19996d0dbea321700ad83d7c000ee1255c966e338863b684fdcd673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Anti-Inflammatory Agents - chemistry</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Cell Line</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Degree of blockiness</topic><topic>Degree of methyl-esterification</topic><topic>Esterification</topic><topic>Esters - chemistry</topic><topic>Esters - metabolism</topic><topic>Hexuronic Acids - chemistry</topic><topic>Humans</topic><topic>Inflammation - metabolism</topic><topic>Macrophages</topic><topic>Pectin</topic><topic>Pectins - chemistry</topic><topic>Pectins - pharmacology</topic><topic>Toll-like receptor 2</topic><topic>Toll-Like Receptor 2 - drug effects</topic><topic>Toll-Like Receptor 2 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beukema, M.</creatorcontrib><creatorcontrib>Jermendi, É.</creatorcontrib><creatorcontrib>van den Berg, M.A.</creatorcontrib><creatorcontrib>Faas, M.M.</creatorcontrib><creatorcontrib>Schols, H.A.</creatorcontrib><creatorcontrib>de Vos, P.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Carbohydrate polymers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beukema, M.</au><au>Jermendi, É.</au><au>van den Berg, M.A.</au><au>Faas, M.M.</au><au>Schols, H.A.</au><au>de Vos, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The impact of the level and distribution of methyl-esters of pectins on TLR2-1 dependent anti-inflammatory responses</atitle><jtitle>Carbohydrate polymers</jtitle><addtitle>Carbohydr Polym</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>251</volume><spage>117093</spage><epage>117093</epage><pages>117093-117093</pages><artnum>117093</artnum><issn>0144-8617</issn><eissn>1879-1344</eissn><abstract>•Homogalacturonan pectins mainly inhibit TLR2-1.•Pectins with a low DM or intermediate DM with a high DB inhibited TLR2-1 strongest.•TLR2 bound strongest to pectins with a low DM or an intermediate DM with a high DB.•TLR2-1 inhibiting pectins also inhibited IL-6 secretion from macrophages.
Pectins have anti-inflammatory effects via Toll-like receptor (TLR) inhibition in a degree of methyl-esterification-(DM)-dependent manner. However, pectins also vary in distribution of methyl-esters over the galacturonic-acid (GalA) backbone (Degree of Blockiness - DB) and impact of this on anti-inflammatory capacity is unknown. Pectins mainly inhibit TLR2-1 but magnitude depends on both DM and DB. Low DM pectins (DM18/19) with both low (DB86) and high DB (DB94) strongly inhibit TLR2-1. However, pectins with intermediate DM (DM43/DM49) and high DB (DB60), but not with low DB (DB33), inhibit TLR2-1 as strongly as low DM. High DM pectins (DM84/88) with DB71 and DB91 do not inhibit TLR2-1 strongly. Pectin-binding to TLR2 was confirmed by capture-ELISA. In human macrophages, low DM and intermediate DM pectins with high DB inhibited TLR2-1 induced IL-6 secretion. Both high number and blockwise distribution of non-esterified GalA in pectins are responsible for the anti-inflammatory effects via inhibition of TLR2-1.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>33152851</pmid><doi>10.1016/j.carbpol.2020.117093</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anti-Inflammatory Agents - chemistry Anti-Inflammatory Agents - pharmacology Cell Line Chromatography, High Pressure Liquid Degree of blockiness Degree of methyl-esterification Esterification Esters - chemistry Esters - metabolism Hexuronic Acids - chemistry Humans Inflammation - metabolism Macrophages Pectin Pectins - chemistry Pectins - pharmacology Toll-like receptor 2 Toll-Like Receptor 2 - drug effects Toll-Like Receptor 2 - metabolism |
| title | The impact of the level and distribution of methyl-esters of pectins on TLR2-1 dependent anti-inflammatory responses |
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