7 results on '"Dias, Greicy Brisa Malaquias"'
Search Results
2. Microbiota-derived acetate protects against respiratory syncytial virus infection through a GPR43-type 1 interferon response
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Antunes, Krist Helen, Fachi, José Luís, de Paula, Rosemeire, da Silva, Emanuelle Fraga, Pral, Laís Passariello, dos Santos, Adara Áurea, Dias, Greicy Brisa Malaquias, Vargas, José Eduardo, Puga, Renato, Mayer, Fabiana Quoos, Maito, Fábio, Zárate-Bladés, Carlos R., Ajami, Nadim J., Sant’Ana, Marcella Ramos, Candreva, Thamiris, Rodrigues, Hosana Gomes, Schmiele, Marcio, Silva Clerici, Maria Teresa Pedrosa, Proença-Modena, José Luiz, Vieira, Angélica Thomas, Mackay, Charles R., Mansur, Daniel, Caballero, Mauricio T., Marzec, Jacqui, Li, Jianying, Wang, Xuting, Bell, Douglas, Polack, Fernando P., Kleeberger, Steven R., Stein, Renato T., Vinolo, Marco Aurélio Ramirez, and de Souza, Ana Paula Duarte
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- 2019
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3. DNA-PKcs restricts Zika virus spreading and is required for effective antiviral response
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Patricio, Daniel De Oliveira, Dias, Greicy Brisa Malaquias, Granella, Lucilene Wildner, Trigg, Ben, Teague, Helena Claire, Bittencourt, Dina, Báfica, André, Zanotto-Filho, Alfeu, Ferguson, Brian, Mansur, Daniel Santos, and Apollo - University of Cambridge Repository
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Zika Virus Infection ,Immunology ,Infant, Newborn ,interferon ,Zika Virus ,DNA ,Virus Replication ,Antiviral Agents ,infection ,Animals ,Humans ,Immunology and Allergy ,Interferons ,DNA-PKcs ,double-strand DNA breaks - Abstract
Peer reviewed: True, Zika virus (ZIKV) is a single-strand RNA mosquito-borne flavivirus with significant public health impact. ZIKV infection induces double-strand DNA breaks (DSBs) in human neural progenitor cells that may contribute to severe neuronal manifestations in newborns. The DNA-PK complex plays a critical role in repairing DSBs and in the innate immune response to infection. It is unknown, however, whether DNA-PK regulates ZIKV infection. Here we investigated the role of DNA-PKcs, the catalytic subunit of DNA-PK, during ZIKV infection. We demonstrate that DNA-PKcs restricts the spread of ZIKV infection in human epithelial cells. Increased ZIKV replication and spread in DNA-PKcs deficient cells is related to a notable decrease in transcription of type I and III interferons as well as IFIT1, IFIT2, and IL6. This was shown to be independent of IRF1, IRF3, or p65, canonical transcription factors necessary for activation of both type I and III interferon promoters. The mechanism of DNA-PKcs to restrict ZIKV infection is independent of DSB. Thus, these data suggest a non-canonical role for DNA-PK during Zika virus infection, acting downstream of IFNs transcription factors for an efficient antiviral immune response.
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- 2022
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4. Desenvolvimento de linhagens TcI e TcII de Trypanosoma cruzi expressando proteínas fluorescentes para estudo da interação parasito-hospedeiro
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Dias, Greicy Brisa Malaquias, Universidade Federal de Santa Catarina, and Steindel, Mario
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Tripanossoma cruzi ,Biotecnologia ,Coinfecção - Abstract
Tese (doutorado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas, Programa de Pós-Graduação em Biotecnologia e Biociências, Florianópolis, 2016. Surtos de doença de Chagas aguda associados à transmissão pela via oral têm sido reportados no Brasil e em outros países da América do Sul. Contudo, estudos sobre a dinâmica da infecção por via oral ainda são incipientes. O presente trabalho teve por objetivo avaliar a interação in vitro e in vivo de linhagens transfectadas de T. cruzi TcI e TcII com plasmídeos pTREXRFP/GFPNeo e pROCKGFPNeo. Para tanto, foram geradas linhagens da cepa SC25 (TcI) e SC96 (TcII) expressando de maneira estável as proteínas fluorescentes RFPe GFP, respectivamente. A cepa Y expressando GFP foi utilizada em ensaios de interação parasito-hospedeiro. Estudos in vitro mostraram que a transfecção não alterou o crescimento e a capacidade de infecção das cepas. Ensaios de co-infecção em células THP-1 mostraram que misturas de parasitos TcI e TcII em diferentes proporções apresentaram níveis de infecção inferiores aos observados para as cepas em infecções isoladas eque uma mesma célula comporta a infecção pelas duas linhagens de parasitos. Triatomíneos infectados isoladamente com cada uma das cepas transfectadas apresentaram taxa de infecção semelhante. Contrariamente, infecções mistas nos insetos mostraram um predomínio de parasitos da linhagem TcII. Em camundongos a infecção pela via oral da cepa TcI não foi capaz de induzir parasitemia sanguínea detectável nos animais. Por outro lado, a cepa YGFP ocasionou parasitemia sanguínea patente e nas inoculações com misturas de TcI e TcII, apenas parasitos TcII foram detectados no sangue e tecidos de animais infectados. O tratamento de tripomastigotas da cepa SC25RFP com pepsina reduziu significativamente sua capacidade de infecção em células THP-1, sugerindo que a passagem pelo ambiente gástrico pode ter interferido negativamente na infecção de camundongos pela via oral. A avaliação histopatológica mostrou que o processo inflamatório na fase aguda foi mais intenso e com presença de parasitismo apenas no tecido cardíaco para a cepa YGFP. Na fase crônica a inflamação foi reduzida e não foram encontrados parasitos visíveis nos tecidos avaliados. Contudo, a PCR revelou a presença de DNA do parasito em todos os tecidos examinados. Os resultados do presente trabalho sugerem que a dinâmica da co-infecção está mais associada às características das cepas de T. cruzi do que a linhagem genética (DTU) à que elas pertencem. Parasitos transfectados expressando genes repórteres distintos pode ser uma ferramenta útil no estudo da dinâmica de infecção mista. Abstract : Acute Chagas' disease outbreaks associated with oral transmission have been reported in Brazil and other South American countries. However, oral infection dynamics studies are still incipient. The present work aimed to evaluate the in vitro and in vivo interaction of T. cruzi TcI and TcII transfected strains with plasmids pTREXRFP / GFPNeo and pROCKGFPNeo. Transfected SC25 (TcI) and SC96 (TcII) strains were showed stable RFP and GFP fluorescent proteins expression, respectively. Y strain expressing GFP was used in parasite-host interaction assays. In vitro studies showed that transfection did not afected the strains growth. Co-infection assays in THP-1 cells showed that mixtures of TcI and TcII parasites in different proportions had lower levels of infection than those observed for the isolated strains and that the same cell carries infection by the two strains of parasites. Triatomines infected with each transfected strains showed a similar infection rate. In contrast, mixed infections showed a predominance of TcII lineage parasites in the insect gut. In mice, oral infection with TcI strainwas not able to induce detectable blood parasitemia in the animals. On the other hand, the YGFP strain caused patent blood parasitemia and in mixed infections only TcII parasites were detected in blood and tissues of infected mice. Treatment of trypomastigotes of the SC25RFP strain with pepsin significantly reduced their ability to infect THP-1 cells, suggesting that passage through the gastric environment may have interfered with the parasite capacity to infect mice by oral route. The histopathological evaluation showed that inflammatory process was more intense in the acute phase and YGFP parasites were detected only in heart. In the chronic phase inflammation was reduced and no visible parasites were found in the evaluatedt issues. However, PCR revealed parasite DNA in all examined tissues. The present work suggest that co-infection dynamics is more associated with the T. cruzi strain characteristics than the genetic lineage (DTU) to which they belong. Transfected parasites expressing different reporter genes may be a useful tool for the study of mixed infection dynamic.
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- 2016
5. Spatial distribution of intestinal parasitic infections in a Kaingáng indigenous village from Southern Brazil
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Da Silva, Joseane Balan, primary, Bossolani, Gleison Daion Piovezana, additional, Piva, Camila, additional, Dias, Greicy Brisa Malaquias, additional, Gomes Ferreira, Jancarlo, additional, Rossoni, Diogo Francisco, additional, Mota, Lúcio Tadeu, additional, and Toledo, Max Jean Ornelas, additional
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- 2016
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6. Evolution of infection in mice inoculated by the oral route with different developmental forms of Trypanosoma cruzi I and II
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Dias, Greicy Brisa Malaquias, primary, Gruendling, Ana Paula, additional, Araújo, Silvana Marques, additional, Gomes, Mônica Lúcia, additional, and Toledo, Max Jean de Ornelas, additional
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- 2013
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7. The Endogenous Retinoic Acid Receptor Pathway Is Exploited by Mycobacterium tuberculosis during Infection, Both In Vitro and In Vivo.
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Tenório de Menezes YK, Eto C, de Oliveira J, Larson EC, Mendes DAGB, Dias GBM, Delgobo M, Gubernat AK, Gleim JL, Munari EL, Starick M, Ferreira F, Mansur DS, Costa DL, Scanga CA, and Báfica A
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- Mice, Humans, Animals, Drug Inverse Agonism, Tretinoin pharmacology, Retinoid X Receptors, Receptors, Retinoic Acid metabolism, Mycobacterium tuberculosis metabolism
- Abstract
Retinoic acid (RA) is a fundamental vitamin A metabolite involved in regulating immune responses through the nuclear RA receptor (RAR) and retinoid X receptor. While performing experiments using THP-1 cells as a model for Mycobacterium tuberculosis infection, we observed that serum-supplemented cultures displayed high levels of baseline RAR activation in the presence of live, but not heat-killed, bacteria, suggesting that M. tuberculosis robustly induces the endogenous RAR pathway. Using in vitro and in vivo models, we have further explored the role of endogenous RAR activity in M. tuberculosis infection through pharmacological inhibition of RARs. We found that M. tuberculosis induces classical RA response element genes such as CD38 and DHRS3 in both THP-1 cells and human primary CD14+ monocytes via a RAR-dependent pathway. M. tuberculosis-stimulated RAR activation was observed with conditioned media and required nonproteinaceous factor(s) present in FBS. Importantly, RAR blockade by (4-[(E)-2-[5,5-dimethyl-8-(2-phenylethynyl)-6H-naphthalen-2-yl]ethenyl]benzoic acid), a specific pan-RAR inverse agonist, in a low-dose murine model of tuberculosis significantly reduced SIGLEC-F+CD64+CD11c+high alveolar macrophages in the lungs, which correlated with 2× reduction in tissue mycobacterial burden. These results suggest that the endogenous RAR activation axis contributes to M. tuberculosis infection both in vitro and in vivo and reveal an opportunity for further investigation of new antituberculosis therapies., (Copyright © 2023 by The American Association of Immunologists, Inc.)
- Published
- 2023
- Full Text
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