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Experimental periodontitis was induced in KO (<jats:italic>lincRNA\u2010EPS<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) and WT (<jats:italic>lincRNA\u2010EPS<\/jats:italic><jats:sup>+\/+<\/jats:sup>) mice to compare the periodontal bone loss and inflammation by using micro\u2010computed tomography, immunofluorescence staining and haematoxylin and eosin staining. The expression and activation of cysteinyl aspartate\u2010specific proteinase\u201011 (caspase\u201011) and NOD\u2010like receptor protein 3 (NLRP3) inflammasomes, as well as nuclear factor\u2010kappa B (NF\u2010\u03baB) activation in mouse gingival fibroblasts (MGFs), were measured by real\u2010time quantitative polymerase chain reaction, Western blotting, enzyme\u2010linked immunosorbent and lactate dehydrogenase assays. MGFs were transfected with overexpression plasmids to assess the biological functions of lincRNA\u2010EPS. RNA pull\u2010down and immunoprecipitation experiments were performed to identify the interacting protein of lincRNA\u2010EPS. LincRNA\u2010EPS\u2010expressing lentivirus was locally administered to inflamed periodontal tissues to evaluate its salvage function in periodontitis. The absence of lincRNA\u2010EPS increased bone loss and expression of myeloperoxidase, interleukin\u20101\u03b1 (IL\u20101\u03b1) and IL\u20101\u03b2 in the inflammatory periodontium. LincRNA\u2010EPS KO MGFs exhibited increased expression and activation of caspase\u201011\/NLRP3 inflammasome components than WT MGFs under lipopolysaccharide (LPS) stimulation. The expression and activation of these molecules were inhibited in lincRNA\u2010EPS overexpressed MGFs. Mechanistically, lincRNA\u2010EPS directly bound to transactive response DNA\u2010binding protein 43 (TDP43) in the nucleus of MGFs, and TDP43 knockdown exerted a similar inhibitory effect on NF\u2010\u03baB activation and the inflammasomes as lincRNA\u2010EPS overexpression. Locally injecting lincRNA\u2010EPS\u2010expressing lentivirus weakened the periodontal damage. LincRNA\u2010EPS inhibits the LPS\u2010induced production and activation of caspase\u201011 and NLRP3 inflammasomes by suppressing the activation of the NF\u2010\u03baB signalling pathway via interacting with TDP43, thereby alleviating periodontitis.<\/jats:p>","DOI":"10.1111\/cpr.13539","type":"journal-article","created":{"date-parts":[[2023,9,15]],"date-time":"2023-09-15T05:06:44Z","timestamp":1694754404000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["LincRNA\u2010EPS inhibits caspase\u201011 and NLRP3 inflammasomes in gingival fibroblasts to alleviate periodontal inflammation"],"prefix":"10.1111","volume":"57","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9138-8578","authenticated-orcid":false,"given":"Anni","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Prosthodontics Stomatological Hospital and Dental School of Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics Stomatological Hospital and Dental School of Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenjing","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics Stomatological Hospital and Dental School of Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huilin","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Prosthodontics Stomatological Hospital and Dental School of Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration Shanghai 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