Regulation of caries‐induced pulp inflammation by NLRP3 inflammasome: A laboratory‐based investigation
Aim To evaluate the expression and function of the nod‐like receptor pyrin domain containing 3 (NLRP3) inflammasome in caries induced pulpitis. Methodology NLRP3 expression was determined with immunohistochemistry in the dental pulp and qPCR in dental pulp cells (DPCs). THP‐1 macrophages expressing...
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| Veröffentlicht in: | International endodontic journal 2023-02, Vol.56 (2), p.193-202 |
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| creator | Al Natour, Banan Lundy, Fionnuala T. About, Imad Jeanneau, Charlotte Dombrowski, Yvonne El Karim, Ikhlas A. |
| description | Aim
To evaluate the expression and function of the nod‐like receptor pyrin domain containing 3 (NLRP3) inflammasome in caries induced pulpitis.
Methodology
NLRP3 expression was determined with immunohistochemistry in the dental pulp and qPCR in dental pulp cells (DPCs). THP‐1 macrophages expressing the apoptosis‐related speck‐like protein (ASC) and green fluorescent protein (GFP) fusion protein were used to assess NLRP3 inflammasome activation by live cell imaging, following treatment with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Caspase I inhibitor was used to confirm inflammasome activation. An ex‐vivo pulpitis model in which the DPCs were co‐cultured with THP‐1 macrophages was used to study the effect of the NLRP3 inflammasome inhibitor (MCC950), and cytokines were measured using ELISA and multiplex array. Data were analysed using the t‐test or anova followed by a Bonferroni post hoc test with the level of significance set at p ≤ .05.
Results
NLRP3 inflammasome was differentially expressed in dental pulp of sound and carious teeth. Treatment of DPCs with LTA significantly upregulates NLRP3 and IL‐1 β‐expression (p |
| doi_str_mv | 10.1111/iej.13855 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10099991</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2729027977</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4785-a321b83df469900ce5278ea4dabd0967e592d83841962664c274f4eb777d84fd3</originalsourceid><addsrcrecordid>eNp1kc1uEzEUhS0EoqGw4AXQSGxgMa3_f9igqCq0KAJUwdryjD2pI884tTNB2fEIPCNPgtMpASpxN5auv3Ourw8AzxE8QaVOvVudICIZewBmiHBWY6bQQzCDiJIaS8mOwJOcVxBCBgl6DI4Ix1JASWZgdeWWYzAbH4cqdlVrknf55_cffrBj62y1HsO68kMXTN9PVLOrPi6uPpNDN8fevanmVTBNTGYT067oG5OL2g9blzd-eat8Ch51JmT37O48Bl_fnX85u6gXn95fns0XdUuFZLUhGDWS2I5ypSBsHcNCOkOtaSxUXDimsJVEUqQ45py2WNCOukYIYSXtLDkGbyff9dj0zrZu2CQT9Dr53qSdjsbrf28Gf62XcasRhKoUKg6vJ4fre7qL-ULve5BSBTkV2z376m5aijdj2Vb3PrcuBDO4OGaNBVYQCyVEQV_eQ1dxTEP5i0IVN0ig4H-GtynmnFx3eAGCeh-3LnHr27gL--LvVQ_k73wLcDoB33xwu_876cvzD5PlLxAntgk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2764703076</pqid></control><display><type>article</type><title>Regulation of caries‐induced pulp inflammation by NLRP3 inflammasome: A laboratory‐based investigation</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Al Natour, Banan ; Lundy, Fionnuala T. ; About, Imad ; Jeanneau, Charlotte ; Dombrowski, Yvonne ; El Karim, Ikhlas A.</creator><creatorcontrib>Al Natour, Banan ; Lundy, Fionnuala T. ; About, Imad ; Jeanneau, Charlotte ; Dombrowski, Yvonne ; El Karim, Ikhlas A.</creatorcontrib><description>Aim
To evaluate the expression and function of the nod‐like receptor pyrin domain containing 3 (NLRP3) inflammasome in caries induced pulpitis.
Methodology
NLRP3 expression was determined with immunohistochemistry in the dental pulp and qPCR in dental pulp cells (DPCs). THP‐1 macrophages expressing the apoptosis‐related speck‐like protein (ASC) and green fluorescent protein (GFP) fusion protein were used to assess NLRP3 inflammasome activation by live cell imaging, following treatment with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Caspase I inhibitor was used to confirm inflammasome activation. An ex‐vivo pulpitis model in which the DPCs were co‐cultured with THP‐1 macrophages was used to study the effect of the NLRP3 inflammasome inhibitor (MCC950), and cytokines were measured using ELISA and multiplex array. Data were analysed using the t‐test or anova followed by a Bonferroni post hoc test with the level of significance set at p ≤ .05.
Results
NLRP3 inflammasome was differentially expressed in dental pulp of sound and carious teeth. Treatment of DPCs with LTA significantly upregulates NLRP3 and IL‐1 β‐expression (p < .05) and in induces more ASC specks formation compared to LPS. IL‐β release in response to LTA treatment is significantly reduced with Caspase I inhibitor suggesting inflammasome dependent mechanism (p < .01). NLRP3‐specific inhibitor, MCC950, significantly reduced IL‐1β and IL‐6 in an ex‐vivo pulpitis model (p < .01) but had no effect on IL‐8 or matrix metalloproteinase‐9 (MMP‐9).
Conclusions
Expression and upregulation of NLRP3 inflammasome with caries and LTA treatment suggest a role in caries‐induced pulpitis. NLRP3 inhibitor attenuated the release of selective inflammatory cytokines and could be a potential treatment target that merit further investigation.</description><identifier>ISSN: 0143-2885</identifier><identifier>EISSN: 1365-2591</identifier><identifier>DOI: 10.1111/iej.13855</identifier><identifier>PMID: 36287083</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Apoptosis ; Biological Research ; caries bacteria ; Caspase ; Caspases ; Cell activation ; Cell death ; Cytokines ; Cytokines - metabolism ; Dental caries ; Dental Caries Susceptibility ; Dental pulp ; Enzyme-linked immunosorbent assay ; Fusion protein ; Green fluorescent protein ; Humans ; Immunohistochemistry ; Inflammasomes ; Inflammasomes - metabolism ; Inflammation ; Inflammation - metabolism ; Interleukin 6 ; Interleukin-1beta - metabolism ; Life Sciences ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Lipoteichoic acid ; Macrophages ; Matrix metalloproteinase ; Metalloproteinase ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 inflammasome ; Original ; Proteins ; pulp death ; Pulpitis ; Pyrin protein ; Sulfonamides ; vital pulp treatment</subject><ispartof>International endodontic journal, 2023-02, Vol.56 (2), p.193-202</ispartof><rights>2022 The Authors. published by John Wiley & Sons Ltd on behalf of British Endodontic Society.</rights><rights>2022 The Authors. International Endodontic Journal published by John Wiley & Sons Ltd on behalf of British Endodontic Society.</rights><rights>2022. This article is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4785-a321b83df469900ce5278ea4dabd0967e592d83841962664c274f4eb777d84fd3</citedby><cites>FETCH-LOGICAL-c4785-a321b83df469900ce5278ea4dabd0967e592d83841962664c274f4eb777d84fd3</cites><orcidid>0000-0003-1732-6288 ; 0000-0002-7453-3921 ; 0000-0002-5314-7378 ; 0000-0003-3150-1150</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fiej.13855$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fiej.13855$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36287083$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04490647$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Al Natour, Banan</creatorcontrib><creatorcontrib>Lundy, Fionnuala T.</creatorcontrib><creatorcontrib>About, Imad</creatorcontrib><creatorcontrib>Jeanneau, Charlotte</creatorcontrib><creatorcontrib>Dombrowski, Yvonne</creatorcontrib><creatorcontrib>El Karim, Ikhlas A.</creatorcontrib><title>Regulation of caries‐induced pulp inflammation by NLRP3 inflammasome: A laboratory‐based investigation</title><title>International endodontic journal</title><addtitle>Int Endod J</addtitle><description>Aim
To evaluate the expression and function of the nod‐like receptor pyrin domain containing 3 (NLRP3) inflammasome in caries induced pulpitis.
Methodology
NLRP3 expression was determined with immunohistochemistry in the dental pulp and qPCR in dental pulp cells (DPCs). THP‐1 macrophages expressing the apoptosis‐related speck‐like protein (ASC) and green fluorescent protein (GFP) fusion protein were used to assess NLRP3 inflammasome activation by live cell imaging, following treatment with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Caspase I inhibitor was used to confirm inflammasome activation. An ex‐vivo pulpitis model in which the DPCs were co‐cultured with THP‐1 macrophages was used to study the effect of the NLRP3 inflammasome inhibitor (MCC950), and cytokines were measured using ELISA and multiplex array. Data were analysed using the t‐test or anova followed by a Bonferroni post hoc test with the level of significance set at p ≤ .05.
Results
NLRP3 inflammasome was differentially expressed in dental pulp of sound and carious teeth. Treatment of DPCs with LTA significantly upregulates NLRP3 and IL‐1 β‐expression (p < .05) and in induces more ASC specks formation compared to LPS. IL‐β release in response to LTA treatment is significantly reduced with Caspase I inhibitor suggesting inflammasome dependent mechanism (p < .01). NLRP3‐specific inhibitor, MCC950, significantly reduced IL‐1β and IL‐6 in an ex‐vivo pulpitis model (p < .01) but had no effect on IL‐8 or matrix metalloproteinase‐9 (MMP‐9).
Conclusions
Expression and upregulation of NLRP3 inflammasome with caries and LTA treatment suggest a role in caries‐induced pulpitis. NLRP3 inhibitor attenuated the release of selective inflammatory cytokines and could be a potential treatment target that merit further investigation.</description><subject>Apoptosis</subject><subject>Biological Research</subject><subject>caries bacteria</subject><subject>Caspase</subject><subject>Caspases</subject><subject>Cell activation</subject><subject>Cell death</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Dental caries</subject><subject>Dental Caries Susceptibility</subject><subject>Dental pulp</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fusion protein</subject><subject>Green fluorescent protein</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Interleukin 6</subject><subject>Interleukin-1beta - metabolism</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Lipoteichoic acid</subject><subject>Macrophages</subject><subject>Matrix metalloproteinase</subject><subject>Metalloproteinase</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3 inflammasome</subject><subject>Original</subject><subject>Proteins</subject><subject>pulp death</subject><subject>Pulpitis</subject><subject>Pyrin protein</subject><subject>Sulfonamides</subject><subject>vital pulp treatment</subject><issn>0143-2885</issn><issn>1365-2591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp1kc1uEzEUhS0EoqGw4AXQSGxgMa3_f9igqCq0KAJUwdryjD2pI884tTNB2fEIPCNPgtMpASpxN5auv3Ourw8AzxE8QaVOvVudICIZewBmiHBWY6bQQzCDiJIaS8mOwJOcVxBCBgl6DI4Ix1JASWZgdeWWYzAbH4cqdlVrknf55_cffrBj62y1HsO68kMXTN9PVLOrPi6uPpNDN8fevanmVTBNTGYT067oG5OL2g9blzd-eat8Ch51JmT37O48Bl_fnX85u6gXn95fns0XdUuFZLUhGDWS2I5ypSBsHcNCOkOtaSxUXDimsJVEUqQ45py2WNCOukYIYSXtLDkGbyff9dj0zrZu2CQT9Dr53qSdjsbrf28Gf62XcasRhKoUKg6vJ4fre7qL-ULve5BSBTkV2z376m5aijdj2Vb3PrcuBDO4OGaNBVYQCyVEQV_eQ1dxTEP5i0IVN0ig4H-GtynmnFx3eAGCeh-3LnHr27gL--LvVQ_k73wLcDoB33xwu_876cvzD5PlLxAntgk</recordid><startdate>202302</startdate><enddate>202302</enddate><creator>Al Natour, Banan</creator><creator>Lundy, Fionnuala T.</creator><creator>About, Imad</creator><creator>Jeanneau, Charlotte</creator><creator>Dombrowski, Yvonne</creator><creator>El Karim, Ikhlas A.</creator><general>Wiley Subscription Services, Inc</general><general>Wiley</general><general>John Wiley and Sons Inc</general><scope>24P</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>7QP</scope><scope>K9.</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1732-6288</orcidid><orcidid>https://orcid.org/0000-0002-7453-3921</orcidid><orcidid>https://orcid.org/0000-0002-5314-7378</orcidid><orcidid>https://orcid.org/0000-0003-3150-1150</orcidid></search><sort><creationdate>202302</creationdate><title>Regulation of caries‐induced pulp inflammation by NLRP3 inflammasome: A laboratory‐based investigation</title><author>Al Natour, Banan ; Lundy, Fionnuala T. ; About, Imad ; Jeanneau, Charlotte ; Dombrowski, Yvonne ; El Karim, Ikhlas A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4785-a321b83df469900ce5278ea4dabd0967e592d83841962664c274f4eb777d84fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Biological Research</topic><topic>caries bacteria</topic><topic>Caspase</topic><topic>Caspases</topic><topic>Cell activation</topic><topic>Cell death</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Dental caries</topic><topic>Dental Caries Susceptibility</topic><topic>Dental pulp</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fusion protein</topic><topic>Green fluorescent protein</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammasomes</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Interleukin 6</topic><topic>Interleukin-1beta - metabolism</topic><topic>Life Sciences</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Lipoteichoic acid</topic><topic>Macrophages</topic><topic>Matrix metalloproteinase</topic><topic>Metalloproteinase</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3 inflammasome</topic><topic>Original</topic><topic>Proteins</topic><topic>pulp death</topic><topic>Pulpitis</topic><topic>Pyrin protein</topic><topic>Sulfonamides</topic><topic>vital pulp treatment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Al Natour, Banan</creatorcontrib><creatorcontrib>Lundy, Fionnuala T.</creatorcontrib><creatorcontrib>About, Imad</creatorcontrib><creatorcontrib>Jeanneau, Charlotte</creatorcontrib><creatorcontrib>Dombrowski, Yvonne</creatorcontrib><creatorcontrib>El Karim, Ikhlas A.</creatorcontrib><collection>Wiley Online Library 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>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</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><jtitle>International endodontic journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Al Natour, Banan</au><au>Lundy, Fionnuala T.</au><au>About, Imad</au><au>Jeanneau, Charlotte</au><au>Dombrowski, Yvonne</au><au>El Karim, Ikhlas A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of caries‐induced pulp inflammation by NLRP3 inflammasome: A laboratory‐based investigation</atitle><jtitle>International endodontic journal</jtitle><addtitle>Int Endod J</addtitle><date>2023-02</date><risdate>2023</risdate><volume>56</volume><issue>2</issue><spage>193</spage><epage>202</epage><pages>193-202</pages><issn>0143-2885</issn><eissn>1365-2591</eissn><abstract>Aim
To evaluate the expression and function of the nod‐like receptor pyrin domain containing 3 (NLRP3) inflammasome in caries induced pulpitis.
Methodology
NLRP3 expression was determined with immunohistochemistry in the dental pulp and qPCR in dental pulp cells (DPCs). THP‐1 macrophages expressing the apoptosis‐related speck‐like protein (ASC) and green fluorescent protein (GFP) fusion protein were used to assess NLRP3 inflammasome activation by live cell imaging, following treatment with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Caspase I inhibitor was used to confirm inflammasome activation. An ex‐vivo pulpitis model in which the DPCs were co‐cultured with THP‐1 macrophages was used to study the effect of the NLRP3 inflammasome inhibitor (MCC950), and cytokines were measured using ELISA and multiplex array. Data were analysed using the t‐test or anova followed by a Bonferroni post hoc test with the level of significance set at p ≤ .05.
Results
NLRP3 inflammasome was differentially expressed in dental pulp of sound and carious teeth. Treatment of DPCs with LTA significantly upregulates NLRP3 and IL‐1 β‐expression (p < .05) and in induces more ASC specks formation compared to LPS. IL‐β release in response to LTA treatment is significantly reduced with Caspase I inhibitor suggesting inflammasome dependent mechanism (p < .01). NLRP3‐specific inhibitor, MCC950, significantly reduced IL‐1β and IL‐6 in an ex‐vivo pulpitis model (p < .01) but had no effect on IL‐8 or matrix metalloproteinase‐9 (MMP‐9).
Conclusions
Expression and upregulation of NLRP3 inflammasome with caries and LTA treatment suggest a role in caries‐induced pulpitis. NLRP3 inhibitor attenuated the release of selective inflammatory cytokines and could be a potential treatment target that merit further investigation.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>36287083</pmid><doi>10.1111/iej.13855</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-1732-6288</orcidid><orcidid>https://orcid.org/0000-0002-7453-3921</orcidid><orcidid>https://orcid.org/0000-0002-5314-7378</orcidid><orcidid>https://orcid.org/0000-0003-3150-1150</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International endodontic journal, 2023-02, Vol.56 (2), p.193-202 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Apoptosis Biological Research caries bacteria Caspase Caspases Cell activation Cell death Cytokines Cytokines - metabolism Dental caries Dental Caries Susceptibility Dental pulp Enzyme-linked immunosorbent assay Fusion protein Green fluorescent protein Humans Immunohistochemistry Inflammasomes Inflammasomes - metabolism Inflammation Inflammation - metabolism Interleukin 6 Interleukin-1beta - metabolism Life Sciences Lipopolysaccharides Lipopolysaccharides - pharmacology Lipoteichoic acid Macrophages Matrix metalloproteinase Metalloproteinase NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Original Proteins pulp death Pulpitis Pyrin protein Sulfonamides vital pulp treatment |
| title | Regulation of caries‐induced pulp inflammation by NLRP3 inflammasome: A laboratory‐based investigation |
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