P-MAPA, a fungi-derived Immunomodulatory compound, Induces a proinflammatory response in a human whole blood model

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dc.contributorLaboratório de Imunoquímicapt_BR
dc.contributor.authorGonçalves, Mariana Torrentept_BR
dc.contributor.authorSquaiella-Baptistao, Carla C.pt_BR
dc.contributor.authorPidde-Queiroz, Gisellept_BR
dc.contributor.authorLopes, Priscila Hesspt_BR
dc.contributor.authorNunes, Iseu da Silvapt_BR
dc.contributor.authorTambourgi, Denise Vilarinhopt_BR
dc.date.accessioned2020-12-17T18:21:52Z-
dc.date.available2020-12-17T18:21:52Z-
dc.date.issued2020-
dc.identifier.citationGonçalves MT, Squaiella-Baptistao CC., Pidde-Queiroz G, Lopes PH, Nunes IS, Tambourgi DV. P-MAPA, a fungi-derived Immunomodulatory compound, Induces a proinflammatory response in a human whole blood model. Mediators Inflamm.. 2020 Nov;2020:83138. doi:10.1155/2020/8831389.pt_BR
dc.identifier.issn0962-9351-
dc.identifier.issn1466-1861-
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/3388-
dc.description.abstractP-MAPA is a complex compound, derived from Aspergillus oryzae cultures, that has shown immunomodulatory properties in infection and cancer animal models. Despite promising results in these models, the mechanisms of cellular activation by P-MAPA, suggested to be Toll-like receptor- (TLR-) dependent, and its effect on human immune cells, remain unclear. Using an ex vivo model of human whole blood, the effects of P-MAPA on complement system activation, production of cytokines, and the expression of complement receptors (CD11b, C5aR, and C3aR), TLR2, TLR4, and the coreceptor CD14 were analyzed in neutrophils and monocytes. P-MAPA induced complement activation in human blood, detected by increased levels of C3a, C5a, and SC5b-9 in plasma. As a consequence, CD11b expression increased and C5aR decreased upon activation, while C3aR expression remained unchanged in leukocytes. TLR2 and TLR4 expressions were not modulated by P-MAPA treatment on neutrophils, but TLR4 expression was reduced in monocytes, while CD14 expression increased in both cell types. P-MAPA also induced the production of TNF-α, IL-8, and IL-12 and oxidative burst, measured by peroxynitrite levels, in human leukocytes. Complement inhibition with compstatin showed that P-MAPA-induced complement activation drives modulation of C5aR, but not of CD11b, suggesting that P-MAPA acts through both complement-dependent and complement-independent mechanisms. Compstatin also significantly reduced the peroxynitrite generation. Altogether, our results show that P-MAPA induced proinflammatory response in human leukocytes, which is partially mediated by complement activation. Our data contribute to elucidate the complement-dependent and complement-independent mechanisms of P-MAPA, which ultimately result in immune cell activation and in its immunomodulatory properties in infection and cancer animal modelspt_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.extent8831389pt_BR
dc.languageengpt_BR
dc.publisherHindawi Pub. Corp.pt_BR
dc.relation.ispartofMediators of Inflammationpt_BR
dc.rightsOpen Accesspt_BR
dc.titleP-MAPA, a fungi-derived Immunomodulatory compound, Induces a proinflammatory response in a human whole blood modelpt_BR
dc.typeArticlept_BR
dc.identifier.doi10.1155/2020/8831389pt_BR
dc.identifier.urlhttps://doi.org/10.1155/2020/8831389pt_BR
dc.contributor.externalFarmabrasilispt_BR
dc.publisher.citySylvaniapt_BR
dc.identifier.citationvolume2020pt_BR
dc.relation.ispartofabbreviatedMediators Inflamm.pt_BR
dc.identifier.citationabntv. 2020, 83138, nov. 2020pt_BR
dc.identifier.citationvancouver2020 Nov;2020:83138pt_BR
dc.publisher.countryUnited Statespt_BR
dc.contributor.butantanGonçalves, Mariana Torrente|:Aluno|:Laboratório de Imunoquímica|:PrimeiroAutorpt_BR
dc.contributor.butantanSquaiella-Baptistão, Carla Cristina|:Pesquisador|:Laboratório de Imunoquímicapt_BR
dc.contributor.butantanPidde-Queiroz, Giselle|:Pesquisador|:Laboratório de Imunoquímicapt_BR
dc.contributor.butantanLopes, Priscila Hess|:Aluno|:Laboratório de Imunoquímicapt_BR
dc.contributor.butantanTambourgi, Denise Vilarinho|:Pesquisador:Docente permanente PPGTOX|:Laboratório de Imunoquímica|:Autor de correspondênciapt_BR
dc.contributor.butantan2013/07467-1pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2013/07467-1pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2012/05306-8pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
item.openairetypeArticle-
item.fulltextCom Texto completo-
item.grantfulltextembargo_29990101-
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