MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria
Autor(a) principal: | |
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Data de Publicação: | 2014 |
Outros Autores: | , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/37343 http://dx.doi.org/10.1128/IAI.01288-13 |
Resumo: | Malaria is a widespread infectious disease caused by the parasite Plasmodium. During pregnancy, malaria infection leads to a range of complications that can affect both the mother and fetus, including stillbirth, infant mortality, and low birth weight. in this study, we utilized a mouse model of placental malaria (PM) infection to determine the importance of the protein MyD88 in the host immune response to Plasmodium during pregnancy. Initially, we demonstrated that Plasmodium berghei NK65GFP adhered to placental tissue via chondroitin sulfate A and induced PM in mice with a C57BL/6 genetic background. To evaluate the involvement of MyD88 in the pathology of PM, we performed a histopathological analysis of placentas obtained from MyD88(-/-) and wild-type (WT) mice following infection on the 19th gestational day. Our data demonstrated that the detrimental placental alterations observed in the infected mice were correlated with the expression of MyD88. Moreover, in the absence of this protein, production of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) was significantly reduced in the infected mice. More importantly, in contrast to fetuses from infected WT mice, which exhibited a reduction in body weight, the fetuses from infected MyD88(-/-) mice did not display significant weight loss compared to their noninfected littermates. in addition, we observed a decrement of maternal care associated with malaria infection, which was attenuated in the MyD88-deficient mice. Collectively, the results of this study illustrate the pivotal importance of the MyD88 signaling pathway in the pathogenesis of placental malaria, thus presenting new possibilities for targeting MyD88 in therapeutic interventions. |
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Barboza, Renato [UNIFESP]Reis, Aramys SilvaSilva, Leandro Gustavo daHasenkamp, LuteroBenevides Pereira, Keitty RaquelSaraiva Camara, Niels OlsenCosta, Fabio Trindade Maranhão [UNIFESP]D'Imperio Lima, Maria ReginaAlvarez, Jose MariaBoscardin, Silvia BeatrizEpiphanio, Sabrina [UNIFESP]Farias Marinho, Claudio RomeroUniversidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)Universidade Estadual de Campinas (UNICAMP)2016-01-24T14:35:11Z2016-01-24T14:35:11Z2014-02-01Infection and Immunity. Washington: Amer Soc Microbiology, v. 82, n. 2, p. 830-838, 2014.0019-9567http://repositorio.unifesp.br/handle/11600/37343http://dx.doi.org/10.1128/IAI.01288-13WOS000330357100034.pdf10.1128/IAI.01288-13WOS:000330357100034Malaria is a widespread infectious disease caused by the parasite Plasmodium. During pregnancy, malaria infection leads to a range of complications that can affect both the mother and fetus, including stillbirth, infant mortality, and low birth weight. in this study, we utilized a mouse model of placental malaria (PM) infection to determine the importance of the protein MyD88 in the host immune response to Plasmodium during pregnancy. Initially, we demonstrated that Plasmodium berghei NK65GFP adhered to placental tissue via chondroitin sulfate A and induced PM in mice with a C57BL/6 genetic background. To evaluate the involvement of MyD88 in the pathology of PM, we performed a histopathological analysis of placentas obtained from MyD88(-/-) and wild-type (WT) mice following infection on the 19th gestational day. Our data demonstrated that the detrimental placental alterations observed in the infected mice were correlated with the expression of MyD88. Moreover, in the absence of this protein, production of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) was significantly reduced in the infected mice. More importantly, in contrast to fetuses from infected WT mice, which exhibited a reduction in body weight, the fetuses from infected MyD88(-/-) mice did not display significant weight loss compared to their noninfected littermates. in addition, we observed a decrement of maternal care associated with malaria infection, which was attenuated in the MyD88-deficient mice. Collectively, the results of this study illustrate the pivotal importance of the MyD88 signaling pathway in the pathogenesis of placental malaria, thus presenting new possibilities for targeting MyD88 in therapeutic interventions.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Inst Ciencias Biomed, Dept Parasitol, BR-05508 São Paulo, BrazilUniv São Paulo, Inst Ciencias Biomed, Dept Imunol, BR-05508 São Paulo, BrazilUniversidade Federal de São Paulo, Inst Ciencias Ambientais Quim & Farmaceut, Dept Ciencias Exatas & Terra, Diadema, BrazilUniversidade Federal de São Paulo, Inst Ciencias Ambientais Quim & Farmaceut, Dept Ciencias Biol, Diadema, BrazilUniv Estadual Campinas, Inst Biol, Dept Genet Evolucao & Bioagentes, Campinas, SP, BrazilUniversidade Federal de São Paulo, Inst Ciencias Ambientais Quim & Farmaceut, Dept Ciencias Exatas & Terra, Diadema, BrazilUniversidade Federal de São Paulo, Inst Ciencias Ambientais Quim & Farmaceut, Dept Ciencias Biol, Diadema, BrazilFAPESP: 2009/53889-0FAPESP: 2009/53256-7FAPESP: 2011/17880-8FAPESP: 2012/02270-2CAPES: AUX-PE-PNPD 2751/2010CAPES: 258/2010CNPq: 475771/2009-5CNPq: 404213/2012Web of Science830-838engAmer Soc MicrobiologyInfection and ImmunityMyD88 Signaling Is Directly Involved in the Development of Murine Placental Malariainfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000330357100034.pdfapplication/pdf2303924${dspace.ui.url}/bitstream/11600/37343/1/WOS000330357100034.pdf01ea09c288bccb05e30149a6816cc3e7MD51open accessTEXTWOS000330357100034.pdf.txtWOS000330357100034.pdf.txtExtracted texttext/plain51031${dspace.ui.url}/bitstream/11600/37343/9/WOS000330357100034.pdf.txt7ad48ee2c66045cd8f30db5fbbdf9c1eMD59open accessTHUMBNAILWOS000330357100034.pdf.jpgWOS000330357100034.pdf.jpgIM Thumbnailimage/jpeg7179${dspace.ui.url}/bitstream/11600/37343/11/WOS000330357100034.pdf.jpg31e8ec464f15ade51a1d6df7cd7d0537MD511open access11600/373432023-06-05 19:34:40.847open accessoai:repositorio.unifesp.br:11600/37343Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-06-05T22:34:40Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria |
title |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria |
spellingShingle |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria Barboza, Renato [UNIFESP] |
title_short |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria |
title_full |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria |
title_fullStr |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria |
title_full_unstemmed |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria |
title_sort |
MyD88 Signaling Is Directly Involved in the Development of Murine Placental Malaria |
author |
Barboza, Renato [UNIFESP] |
author_facet |
Barboza, Renato [UNIFESP] Reis, Aramys Silva Silva, Leandro Gustavo da Hasenkamp, Lutero Benevides Pereira, Keitty Raquel Saraiva Camara, Niels Olsen Costa, Fabio Trindade Maranhão [UNIFESP] D'Imperio Lima, Maria Regina Alvarez, Jose Maria Boscardin, Silvia Beatriz Epiphanio, Sabrina [UNIFESP] Farias Marinho, Claudio Romero |
author_role |
author |
author2 |
Reis, Aramys Silva Silva, Leandro Gustavo da Hasenkamp, Lutero Benevides Pereira, Keitty Raquel Saraiva Camara, Niels Olsen Costa, Fabio Trindade Maranhão [UNIFESP] D'Imperio Lima, Maria Regina Alvarez, Jose Maria Boscardin, Silvia Beatriz Epiphanio, Sabrina [UNIFESP] Farias Marinho, Claudio Romero |
author2_role |
author author author author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade de São Paulo (USP) Universidade Federal de São Paulo (UNIFESP) Universidade Estadual de Campinas (UNICAMP) |
dc.contributor.author.fl_str_mv |
Barboza, Renato [UNIFESP] Reis, Aramys Silva Silva, Leandro Gustavo da Hasenkamp, Lutero Benevides Pereira, Keitty Raquel Saraiva Camara, Niels Olsen Costa, Fabio Trindade Maranhão [UNIFESP] D'Imperio Lima, Maria Regina Alvarez, Jose Maria Boscardin, Silvia Beatriz Epiphanio, Sabrina [UNIFESP] Farias Marinho, Claudio Romero |
description |
Malaria is a widespread infectious disease caused by the parasite Plasmodium. During pregnancy, malaria infection leads to a range of complications that can affect both the mother and fetus, including stillbirth, infant mortality, and low birth weight. in this study, we utilized a mouse model of placental malaria (PM) infection to determine the importance of the protein MyD88 in the host immune response to Plasmodium during pregnancy. Initially, we demonstrated that Plasmodium berghei NK65GFP adhered to placental tissue via chondroitin sulfate A and induced PM in mice with a C57BL/6 genetic background. To evaluate the involvement of MyD88 in the pathology of PM, we performed a histopathological analysis of placentas obtained from MyD88(-/-) and wild-type (WT) mice following infection on the 19th gestational day. Our data demonstrated that the detrimental placental alterations observed in the infected mice were correlated with the expression of MyD88. Moreover, in the absence of this protein, production of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) was significantly reduced in the infected mice. More importantly, in contrast to fetuses from infected WT mice, which exhibited a reduction in body weight, the fetuses from infected MyD88(-/-) mice did not display significant weight loss compared to their noninfected littermates. in addition, we observed a decrement of maternal care associated with malaria infection, which was attenuated in the MyD88-deficient mice. Collectively, the results of this study illustrate the pivotal importance of the MyD88 signaling pathway in the pathogenesis of placental malaria, thus presenting new possibilities for targeting MyD88 in therapeutic interventions. |
publishDate |
2014 |
dc.date.issued.fl_str_mv |
2014-02-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:35:11Z |
dc.date.available.fl_str_mv |
2016-01-24T14:35:11Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/article |
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article |
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publishedVersion |
dc.identifier.citation.fl_str_mv |
Infection and Immunity. Washington: Amer Soc Microbiology, v. 82, n. 2, p. 830-838, 2014. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/37343 http://dx.doi.org/10.1128/IAI.01288-13 |
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0019-9567 |
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WOS000330357100034.pdf |
dc.identifier.doi.none.fl_str_mv |
10.1128/IAI.01288-13 |
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WOS:000330357100034 |
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Infection and Immunity. Washington: Amer Soc Microbiology, v. 82, n. 2, p. 830-838, 2014. 0019-9567 WOS000330357100034.pdf 10.1128/IAI.01288-13 WOS:000330357100034 |
url |
http://repositorio.unifesp.br/handle/11600/37343 http://dx.doi.org/10.1128/IAI.01288-13 |
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830-838 |
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Amer Soc Microbiology |
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Amer Soc Microbiology |
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