
P-MAPA, a fungi-derived Immunomodulatory compound, Induces a proinflammatory response in a human whole blood model
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DC Field | Value | Language |
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dc.contributor | (LBI) Lab. Imunoquímica | pt_BR |
dc.contributor.author | Gonçalves, Mariana Torrente | pt_BR |
dc.contributor.author | Squaiella-Baptistão, Carla Cristina | pt_BR |
dc.contributor.author | Pidde-Queiroz, Giselle | pt_BR |
dc.contributor.author | Lopes, Priscila Hess | pt_BR |
dc.contributor.author | Nunes, Iseu da Silva | pt_BR |
dc.contributor.author | Tambourgi, Denise Vilarinho | pt_BR |
dc.date.accessioned | 2020-12-17T18:21:52Z | - |
dc.date.available | 2020-12-17T18:21:52Z | - |
dc.date.issued | 2020 | pt_BR |
dc.identifier.citation | Gonçalves 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.uri | https://repositorio.butantan.gov.br/handle/butantan/3388 | - |
dc.description.abstract | P-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 models | pt_BR |
dc.description.sponsorship | (FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo | pt_BR |
dc.description.sponsorship | (CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológico | pt_BR |
dc.format.extent | 8831389 | pt_BR |
dc.language.iso | English | pt_BR |
dc.relation.ispartof | Mediators of Inflammation | pt_BR |
dc.rights | Open access | pt_BR |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | pt_BR |
dc.title | P-MAPA, a fungi-derived Immunomodulatory compound, Induces a proinflammatory response in a human whole blood model | pt_BR |
dc.type | Article | pt_BR |
dc.rights.license | CC BY | pt_BR |
dc.identifier.doi | 10.1155/2020/8831389 | pt_BR |
dc.identifier.url | https://doi.org/10.1155/2020/8831389 | pt_BR |
dc.contributor.external | Farmabrasilis | pt_BR |
dc.identifier.citationvolume | 2020 | pt_BR |
dc.relation.ispartofabbreviated | Mediators Inflamm | pt_BR |
dc.identifier.citationabnt | v. 2020, 83138, nov. 2020 | pt_BR |
dc.identifier.citationvancouver | 2020 Nov;2020:83138 | pt_BR |
dc.contributor.butantan | Gonçalves, Mariana Torrente|:Aluno|:Lab. Imunoquímica|:PrimeiroAutor | pt_BR |
dc.contributor.butantan | Squaiella-Baptistão, Carla Cristina|:Pesquisador|:Lab. Imunoquímica | pt_BR |
dc.contributor.butantan | Pidde-Queiroz, Giselle|:Pesquisador|:Lab. Imunoquímica | pt_BR |
dc.contributor.butantan | Lopes, Priscila Hess|:Aluno|:Lab. Imunoquímica | pt_BR |
dc.contributor.butantan | Tambourgi, Denise Vilarinho|:Pesquisador:Docente permanente PPGTOX|:Lab. Imunoquímica|:Autor de correspondência | pt_BR |
dc.sponsorship.butantan | Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2013/07467-1 | pt_BR |
dc.sponsorship.butantan | Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2012/05306-8 | pt_BR |
dc.sponsorship.butantan | Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦ | pt_BR |
dc.identifier.bvscc | BR78.1 | pt_BR |
dc.identifier.bvsdb | IBProd | pt_BR |
dc.description.dbindexed | Yes | pt_BR |
item.grantfulltext | open | - |
item.languageiso639-1 | English | - |
item.fulltext | Com Texto completo | - |
item.openairetype | Article | - |
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crisitem.author.orcid | #PLACEHOLDER_PARENT_METADATA_VALUE# | - |
crisitem.author.orcid | 0000-0002-4187-798X | - |
crisitem.author.orcid | 0000-0002-7622-5981 | - |
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crisitem.author.orcid | 0000-0003-1896-9074 | - |
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