TLR4-Mediated Placental Pathology and Pregnancy Outcome in Experimental Malaria

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dc.contributor.author Barboza, Renato [UNIFESP]
dc.contributor.author Lima, Flavia Afonso
dc.contributor.author Reis, Aramys Silva
dc.contributor.author Murillo, Oscar Javier
dc.contributor.author Machado Peixoto, Erika Paula
dc.contributor.author Bandeira, Carla Leticia
dc.contributor.author Fotoran, Wesley Luzetti
dc.contributor.author Sardinha, Luis Roberto
dc.contributor.author Wunderlich, Gerhard
dc.contributor.author Bevilacqua, Estela
dc.contributor.author D'Imperio Lima, Maria Regina
dc.contributor.author Alvarez, Jose Maria
dc.contributor.author Maranhao Costa, Fabio Trindade
dc.contributor.author Goncalves, Ligia Antunes
dc.contributor.author Epiphanio, Sabrina
dc.contributor.author Farias Marinho, Cludio Romerso
dc.date.accessioned 2019-08-19T11:49:43Z
dc.date.available 2019-08-19T11:49:43Z
dc.date.issued 2017
dc.identifier http://dx.doi.org/10.1038/s41598-017-08299-x
dc.identifier.citation Scientific Reports. London, v. 7, p. -, 2017.
dc.identifier.issn 2045-2322
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/51385
dc.description.abstract Malaria-associate pregnancy has a significant impact on infant morbidity and mortality. The detrimental effects of malaria infection during pregnancy have been shown to correlate with immune activation in the placental tissue. Herein we sought to evaluate the effect of Toll-like receptors (TLRs) activation on placental malaria (PM) development by using the Plasmodium berghei NK65(GFP) infection model. We observed that activation of the innate immune system by parasites leads to PM due to local inflammation. We identified TLR4 activation as the main pathway involved in the inflammatory process in the placental tissue since the absence of functional TLR4 in mice leads to a decrease in the pro-inflammatory responses, which resulted in an improved pregnancy outcome. Additionally, a similar result was obtained when infected pregnant mice were treated with IAXO-101, a TLR4/CD14 blocker. Together, this study illustrates the importance of TLR4 signalling for the generation of the severe inflammatory response involved in PM pathogenesis. Therefore, our results implicate that TLR4 blockage could be a potential candidate for therapeutic interventions to reduce malaria-induced pathology both in the mother and the fetus. en
dc.description.sponsorship Fundação de Amparo a Pesquisa do Estado de São Paulo - FAPESP
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico - CNPq
dc.format.extent -
dc.language.iso eng
dc.publisher Nature Publishing Group
dc.rights Acesso aberto
dc.title TLR4-Mediated Placental Pathology and Pregnancy Outcome in Experimental Malaria en
dc.type Artigo
dc.description.affiliation Univ Fed São Paulo, Dept Ciencias Biol, Diadema, Brazil
dc.description.affiliation Univ São Paulo, Inst Ciencias Biomed, Dept Parasitol, São Paulo, Brazil
dc.description.affiliation Hosp Israelita Albert Einstein, São Paulo, Brazil
dc.description.affiliation Univ São Paulo, Inst Ciencias Biomed, Dept Biol Celular & Desenvolvimento, São Paulo, Brazil
dc.description.affiliation Univ Estadual Campinas, Dept Genet Evolucao & Bioagentes, Inst Biol, Campinas, SP, Brazil
dc.description.affiliation Univ São Paulo, Inst Ciencias Biomed, Dept Imunol, São Paulo, Brazil
dc.description.affiliation Univ São Paulo, Dept Analises Clin & Toxicol, Fac Ciencias Farmaceut, São Paulo, Brazil
dc.description.affiliationUnifesp Univ Fed São Paulo, Dept Ciencias Biol, Diadema, Brazil
dc.description.sponsorshipID FAPESP: 2009/53889-0
dc.description.sponsorshipID FAPESP: 2014/09964-5
dc.description.sponsorshipID FAPESP: 2014/20451-0
dc.description.sponsorshipID FAPESP: 2012/16525-2
dc.description.sponsorshipID FAPESP: 2011/17880-8
dc.description.sponsorshipID FAPESP: 2013/16417-8
dc.description.sponsorshipID FAPESP: 2011/19048-8
dc.description.sponsorshipID FAPESP: 2013/00981-1
dc.description.sponsorshipID FAPESP: 2015/06106-0]
dc.description.sponsorshipID CAPES: AUX-PE-PNPD 2751/2010
dc.description.sponsorshipID CNPq: 475771/2009-5
dc.identifier.file WOS000407864400004.pdf
dc.identifier.doi 10.1038/s41598-017-08299-x
dc.description.source Web of Science
dc.identifier.wos WOS:000407864400004



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