Natterin an aerolysin-like fish toxin drives IL-1β-dependent neutrophilic inflammation mediated by caspase-1 and caspase-11 activated by the inflammasome sensor NLRP6

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dc.contributorLaboratório de Toxinologia Aplicadapt_BR
dc.contributorCentro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)pt_BR
dc.contributor.authorLima, Carlapt_BR
dc.contributor.authorFalcão, Maria Alice Pimentelpt_BR
dc.contributor.authorAndrade‐Barros, Aline Ingridpt_BR
dc.contributor.authorSeni-Silva, Ana Carolina dept_BR
dc.contributor.authorGrund, Lidiane Zitopt_BR
dc.contributor.authorBalogh, Enikopt_BR
dc.contributor.authorConceiçao, Katiapt_BR
dc.contributor.authorQueniaux, Valerie F.pt_BR
dc.contributor.authorRyffel, Bernhardpt_BR
dc.contributor.authorLopes-Ferreira, Monicapt_BR
dc.date.accessioned2021-01-05T19:30:40Z-
dc.date.available2021-01-05T19:30:40Z-
dc.date.issued2021pt_BR
dc.identifier.citationLima C, Falcão MAP, Barros AIA, Seni-Silva AC, Grund LZ, Balogh E, et al. Natterin an aerolysin-like fish toxin drives IL-1β-dependent neutrophilic inflammation mediated by caspase-1 and caspase-11 activated by the inflammasome sensor NLRP6. Int. Immunopharmacol.. 2021 Feb;91:107287. doi:10.1016/j.intimp.2020.107287.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/3429-
dc.description.abstractNatterin is an aerolysin-like pore-forming toxin responsible for the toxic effects of the venom of the medically significant fish Thalassophryne nattereri. Using a combination of pharmacologic and genetic loss-of-function approaches we conduct a systematic investigation of the regulatory mechanisms that control Natterin-induced neutrophilic inflammation in the peritonitis model. Our data confirmed the capacity of Natterin to induce a strong and sustained neutrophilic inflammation leading to systemic inflammatory lung infiltration and revealed overlapping regulatory paths in its control. We found that Natterin induced the extracellular release of mature IL-1β and the sustained production of IL-33 by bronchial epithelial cells. We confirmed the dependence of both ST2/IL-33 and IL-17A/IL-17RA signaling on the local and systemic neutrophils migration, as well as the crucial role of IL-1α, caspase-1 and caspase-11 for neutrophilic inflammation. The inflammation triggered by Natterin was a gasdermin-D-dependent inflammasome process, despite the cells did not die by pyroptosis. Finally, neutrophilic inflammation was mediated by non-canonical NLRP6 and NLRC4 adaptors through ASC interaction, independent of NLRP3. Our data highlight that the inflammatory process dependent on non-canonical inflammasome activation can be a target for pharmacological intervention in accidents by T. nattereri, which does not have adequate specific therapy.pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorshipCentre National de la Recherche Scientifique (CNRS)pt_BR
dc.format.extent107287pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofInternational Immunopharmacologypt_BR
dc.rightsOpen accesspt_BR
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/pt_BR
dc.titleNatterin an aerolysin-like fish toxin drives IL-1β-dependent neutrophilic inflammation mediated by caspase-1 and caspase-11 activated by the inflammasome sensor NLRP6pt_BR
dc.typeArticlept_BR
dc.rights.licenseCC BY-NC-NDpt_BR
dc.identifier.doi10.1016/j.intimp.2020.107287pt_BR
dc.identifier.urlhttps://doi.org/10.1016/j.intimp.2020.107287pt_BR
dc.contributor.externalUniversity of Debrecenpt_BR
dc.contributor.externalUniversidade Federal de São Paulo (UNIFESP)pt_BR
dc.contributor.externalUniversity Orléanspt_BR
dc.identifier.citationvolume91pt_BR
dc.subject.keywordNatterinpt_BR
dc.subject.keywordAerolysinpt_BR
dc.subject.keywordNeutrophiliapt_BR
dc.subject.keywordNLPR6/NLRC4pt_BR
dc.subject.keywordCaspase-11/caspase-1pt_BR
dc.subject.keywordIL-1α/βpt_BR
dc.relation.ispartofabbreviatedInt Immunopharmacolpt_BR
dc.identifier.citationabntv. 91, 107287, fev. 2021pt_BR
dc.identifier.citationvancouver2021 Feb;91:107287pt_BR
dc.contributor.butantanLima, Carla|:Pesquisador:Docente permanente PPGTOX|:Laboratório de Toxinologia Aplicada:Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)|:PrimeiroAutor:Autor de correspondênciapt_BR
dc.contributor.butantanFalcão, Maria Alice Pimentel|:Aluno|:Laboratório de Toxinologia Aplicada:Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICSpt_BR
dc.contributor.butantanAndrade‐Barros, Aline Ingrid|:Técnico|:Laboratório de Toxinologia Aplicada:Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICSpt_BR
dc.contributor.butantanSeni-Silva, Ana Carolina de|:Aluno|:Laboratório de Toxinologia Aplicada:Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICSpt_BR
dc.contributor.butantanGrund, Lidiane Zito|:Aluno|:Laboratório de Toxinologia Aplicada:Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICSpt_BR
dc.contributor.butantanLopes-Ferreira, Monica|:Pesquisador|:Laboratório de Toxinologia Aplicada:Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICSpt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2019/10500-7pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2018/17413-0pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2013/07467-1pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦pt_BR
dc.sponsorship.butantanCentre National de la Recherche Scientifique (CNRS)¦¦2016-00110366pt_BR
dc.sponsorship.butantanCentre National de la Recherche Scientifique (CNRS)¦¦EX005756pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
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