Natterin-induced neutrophilia is dependent on cGAS/STING activation via type i IFN signaling pathway

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dc.contributorLab. de Toxinologia Aplicadapt_BR
dc.contributorCeTICS - Centro de Toxinas, Resposta-imune e Sinalização Celularpt_BR
dc.contributor.authorLima, Carlapt_BR
dc.contributor.authorAndrade‐Barros, Aline Ingridpt_BR
dc.contributor.authorBernardo, Jefferson Thiago Gonçalvespt_BR
dc.contributor.authorBalogh, Enikopt_BR
dc.contributor.authorQuesniaux, Valerie F.pt_BR
dc.contributor.authorRyffel, Bernhardpt_BR
dc.contributor.authorLopes-Ferreira, Monicapt_BR
dc.date.accessioned2022-04-18T14:55:45Z-
dc.date.available2022-04-18T14:55:45Z-
dc.date.issued2022pt_BR
dc.identifier.citationLima C, Andrade‐Barros AI, Bernardo JTG, Balogh E, Quesniaux VF., Ryffel B, et al. Natterin-induced Neutrophilia is dependent on cGAS/STING activation via type i IFN signaling pathway. Int. J. Mol. Sci. 2022 Mar;23(7):3600. doi:10.3390/ijms23073600.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/4295-
dc.description.abstractNatterin is a potent pro-inflammatory fish molecule, inducing local and systemic IL-1β/IL-1R1-dependent neutrophilia mediated by non-canonical NLRP6 and NLRC4 inflammasome activation in mice, independent of NLRP3. In this work, we investigated whether Natterin activates mitochondrial damage, resulting in self-DNA leaks into the cytosol, and whether the DNA sensor cGAS and STING pathway participate in triggering the innate immune response. Employing a peritonitis mouse model, we found that the deficiency of the tlr2/tlr4, myd88 and trif results in decreased neutrophil influx to peritoneal cavities of mice, indicative that in addition to MyD88, TRIF contributes to neutrophilia triggered by TLR4 engagement by Natterin. Next, we demonstrated that gpcr91 deficiency in mice abolished the neutrophil recruitment after Natterin injection, but mice pre-treated with 2-deoxy-d-glucose that blocks glycolysis presented similar infiltration than WT Natterin-injected mice. In addition, we observed that, compared with the WT Natterin-injected mice, DPI and cyclosporin A treated mice had a lower number of neutrophils in the peritoneal exudate. The levels of dsDNA in the supernatant of the peritoneal exudate and processed IL-33 in the supernatant of the peritoneal exudate or cytoplasmic supernatant of the peritoneal cell lysate of WT Natterin-injected mice were several folds higher than those of the control mice. The recruitment of neutrophils to peritoneal cavity 2 h post-Natterin injection was intensely impaired in ifnar KO mice and partially in il-28r KO mice, but not in ifnγr KO mice. Finally, using cgas KO, sting KO, or irf3 KO mice we found that recruitment of neutrophils to peritoneal cavities was virtually abolished in response to Natterin. These findings reveal cytosolic DNA sensors as critical regulators for Natterin-induced neutrophilia.pt_BR
dc.description.sponsorship(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.description.sponsorship(CNRS) Centre National de la Recherche Scientifiquept_BR
dc.description.sponsorshipRegion Centre-Val de Loirept_BR
dc.format.extent3600pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofInternational Journal of Molecular Sciencespt_BR
dc.rightsOpen accesspt_BR
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/pt_BR
dc.titleNatterin-induced neutrophilia is dependent on cGAS/STING activation via type i IFN signaling pathwaypt_BR
dc.typeArticlept_BR
dc.rights.licenseCC BYpt_BR
dc.identifier.doi10.3390/ijms23073600pt_BR
dc.identifier.urlhttps://doi.org/10.3390/ijms23073600pt_BR
dc.contributor.externalUniversity of Debrecenpt_BR
dc.contributor.externalUniversity Orléanspt_BR
dc.identifier.citationvolume23pt_BR
dc.identifier.citationissue7pt_BR
dc.subject.keywordnatterinpt_BR
dc.subject.keywordneutrophiliapt_BR
dc.subject.keywordself-DNApt_BR
dc.subject.keywordcGAS/STING/IRF3 pathwaypt_BR
dc.subject.keywordtype I IFN signalingpt_BR
dc.relation.ispartofabbreviatedInt. J. Mol. Scipt_BR
dc.identifier.citationabntv. 23, n. 7, 3600, mar. 2022pt_BR
dc.identifier.citationvancouver2022 Mar;23(7):3600pt_BR
dc.contributor.butantanLima, Carla|:Pesquisador:Docente permanente PPGTOX|:Lab. de Toxinologia Aplicada:CeTICS - Centro de Toxinas, Resposta-imune e Sinalização Celular|:Autor de correspondênciapt_BR
dc.contributor.butantanAndrade‐Barros, Aline Ingrid|:Técnico|:Lab. de Toxinologia Aplicada:CeTICS - Centro de Toxinas, Resposta-imune e Sinalização Celularpt_BR
dc.contributor.butantanBernardo, Jefferson Thiago Gonçalves|:Outros|:Lab. de Toxinologia Aplicada:CeTICS - Centro de Toxinas, Resposta-imune e Sinalização Celularpt_BR
dc.contributor.butantanLopes-Ferreira, Monica|:Pesquisador|:Docente Permanente PPGTox|:Lab. de Toxinologia Aplicada:CeTICS - Centro de Toxinas, Resposta-imune e Sinalização Celularpt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦2021/06084-8pt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦2019/10500-7pt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦2018/17413-0pt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦2013/07467-1pt_BR
dc.sponsorship.butantan(CNRS) Centre National de la Recherche Scientifique¦¦pt_BR
dc.sponsorship.butantanRegion Centre-Val de Loire¦¦FEDER EX016008 TARGET-Expt_BR
dc.sponsorship.butantanRegion Centre-Val de Loire¦¦EX010381 EURo-FéRIpt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
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