C5a-C5aR1 axis activation drives envenomation immunopathology by the snake naja annulifera

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dc.contributorLab. Imunoquímicapt_BR
dc.contributor.authorFrança, Felipe Silva dept_BR
dc.contributor.authorVillas-Boas, Isadora Mariapt_BR
dc.contributor.authorCogliati, Brunopt_BR
dc.contributor.authorWoodruff, Trent M.pt_BR
dc.contributor.authorReis, Edimara da Silvapt_BR
dc.contributor.authorLambris, John D.pt_BR
dc.contributor.authorTambourgi, Denise Vilarinhopt_BR
dc.date.accessioned2021-05-06T14:27:52Z-
dc.date.available2021-05-06T14:27:52Z-
dc.date.issued2021pt_BR
dc.identifier.citationFrança FS, Villas-Boas IM, Cogliati B, Woodruff TM., Reis ES, Lambris JD., et al. C5a-C5aR1 axis activation drives envenomation immunopathology by the snake naja annulifera. Front Immunol. 2021 Apr;12:652242. doi:10.3389/fimmu.2021.652242.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/3698-
dc.description.abstractSystemic complement activation drives a plethora of pathological conditions, but its role in snake envenoming remains obscure. Here, we explored complement’s contribution to the physiopathogenesis of Naja annulifera envenomation. We found that N. annulifera venom promoted the generation of C3a, C4a, C5a, and the soluble Terminal Complement Complex (sTCC) mediated by the action of snake venom metalloproteinases. N. annulifera venom also induced the release of lipid mediators and chemokines in a human whole-blood model. This release was complement-mediated, since C3/C3b and C5a Receptor 1 (C5aR1) inhibition mitigated the effects. In an experimental BALB/c mouse model of envenomation, N. annulifera venom promoted lipid mediator and chemokine production, neutrophil influx, and swelling at the injection site in a C5a-C5aR1 axis-dependent manner. N. annulifera venom induced systemic complementopathy and increased interleukin and chemokine production, leukocytosis, and acute lung injury (ALI). Inhibition of C5aR1 with the cyclic peptide antagonist PMX205 rescued mice from these systemic reactions and abrogated ALI development. These data reveal hitherto unrecognized roles for complement in envenomation physiopathogenesis, making complement an interesting therapeutic target in envenomation by N. annulifera and possibly by other snake venoms.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.format.extent652242pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofFrontiers in Immunologypt_BR
dc.rightsOpen Accesspt_BR
dc.titleC5a-C5aR1 axis activation drives envenomation immunopathology by the snake naja annuliferapt_BR
dc.typeArticlept_BR
dc.identifier.doi10.3389/fimmu.2021.652242pt_BR
dc.identifier.urlhttps://doi.org/10.3389/fimmu.2021.652242pt_BR
dc.contributor.externalUniversidade de São Paulo (USP)pt_BR
dc.contributor.externalUniversity of Queensland (UQ)pt_BR
dc.contributor.externalUniversity of Pennsylvaniapt_BR
dc.identifier.citationvolume12pt_BR
dc.subject.keywordNaja snake venompt_BR
dc.subject.keywordenvenomationpt_BR
dc.subject.keywordcomplement systempt_BR
dc.subject.keywordC5a-C5aR1pt_BR
dc.subject.keywordcomplement inhibitorspt_BR
dc.relation.ispartofabbreviatedFront Immunolpt_BR
dc.identifier.citationabntv. 12, 652242, abr. 2021pt_BR
dc.identifier.citationvancouver2021 Apr;12:652242pt_BR
dc.contributor.butantanFrança, Felipe Silva de|:Aluno|:Lab. Imunoquímica|:PrimeiroAutorpt_BR
dc.contributor.butantanVillas-Boas, Isadora Maria|:Aluno|:Lab. Imunoquímicapt_BR
dc.contributor.butantanTambourgi, Denise Vilarinho|:Pesquisador:Docente permanente PPGTOX|:Lab. Imunoquímica|:Autor de correspondênciapt_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)¦¦301358/2017-6pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
item.grantfulltextopen-
item.languageiso639-1English-
item.openairetypeArticle-
item.fulltextCom Texto completo-
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