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22 results on '"Ribeiro‐Gomes, Flávia L."'

3. Thymic Microenvironment Is Modified by Malnutrition and Leishmania infantum Infection

Author

Losada-Barragán, Monica, primary, Umaña-Pérez, Adriana, additional, Durães, Jonathan, additional, Cuervo-Escobar, Sergio, additional, Rodríguez-Vega, Andrés, additional, Ribeiro-Gomes, Flávia L., additional, Berbert, Luiz R., additional, Morgado, Fernanda, additional, Porrozzi, Renato, additional, Mendes-da-Cruz, Daniella Arêas, additional, Aquino, Priscila, additional, Carvalho, Paulo C., additional, Savino, Wilson, additional, Sánchez-Gómez, Myriam, additional, Padrón, Gabriel, additional, and Cuervo, Patricia, additional

Published
2019
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9. Interactions with apoptotic but not with necrotic neutrophils increase parasite burden in human macrophages infected withLeishmania amazonensis

Author

Afonso, Lilian, primary, Borges, Valéria M, additional, Cruz, Heloísa, additional, Ribeiro-Gomes, Flávia L, additional, DosReis, George A, additional, Dutra, Alberto Noronha, additional, Clarêncio, Jorge, additional, de Oliveira, Camila I, additional, Barral, Aldina, additional, Barral-Netto, Manoel, additional, and Brodskyn, Cláudia I, additional

Published
2008
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14. Caspase-8 Activity Prevents Type 2 Cytokine Responses and Is Required for Protective T Cell-Mediated Immunity against Trypanosoma cruzi Infection

Author

Silva, Elisabeth M., primary, Guillermo, Landi V. C., additional, Ribeiro-Gomes, Flávia L., additional, De Meis, Juliana, additional, Pereira, Renata M. S., additional, Wu, Zhengqi, additional, Calegari-Silva, Teresa C., additional, Seabra, Sérgio H., additional, Lopes, Ulisses G., additional, Siegel, Richard M., additional, DosReis, George A., additional, and Lopes, Marcela F., additional

Published
2005
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15. Macrophage Interactions with Neutrophils RegulateLeishmania majorInfection

Author

Ribeiro-Gomes, Flávia L., primary, Otero, Ana C., additional, Gomes, Nitza A., additional, Moniz-de-Souza, Maria Carolina A., additional, Cysne-Finkelstein, Lea, additional, Arnholdt, Andrea C., additional, Calich, Vera L., additional, Coutinho, Sergio G., additional, Lopes, Marcela F., additional, and DosReis, George A., additional

Published
2004
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16. Infection with Leishmania major Induces a Cellular Stress Response in Macrophages.

Author

Filardy, Alessandra A., Costa-da-Silva, Ana Caroline, Koeller, Carolina M., Guimarães-Pinto, Kamila, Ribeiro-Gomes, Flávia L., Lopes, Marcela F., Heise, Norton, Freire-de-Lima, Célio G., Nunes, Marise P., and DosReis, George A.

Subjects
LEISHMANIA major, PROTOZOAN diseases, MACROPHAGES, LABORATORY mice, REACTIVE oxygen species, INFLAMMATION, N-terminal residues, PROTEIN kinases
Abstract

We investigated early cellular responses induced by infection with Leishmania major in macrophages from resistant C57/BL6 mice. Infection increased production of reactive oxygen species by resident, but not inflammatory peritoneal macrophages. In addition, infection increased activation of stress-activated protein kinases/c-Jun N-terminal kinases (SAPK/JNK) in resident, but not in inflammatory peritoneal macrophages. Infection also increased expression of membrane and soluble FasL, but infected macrophages remained viable after 48 h. Infection increased secretion of cytokines/chemokines TNF-α, IL-6, TIMP-1, IL-1RA, G-CSF, TREM, KC, MIP-1α, MIP-1β, MCP-1, and MIP-2 in resident macrophages. Addition of antioxidants deferoxamine and N-acetylcysteine reduced ROS generation and JNK activation. Addition of antioxidants or JNK inhibitor SP600125 reduced secretion of KC. Furthermore, treatment with antioxidants or JNK inhibitor also reduced intracellular parasite replication. These results indicated that infection triggers a rapid cellular stress response in resident macrophages which induces proinflammatory signals, but is also involved in parasite survival and replication in host macrophages. [ABSTRACT FROM AUTHOR]

Published
2014
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18. Inhibition of caspase‐8 activity promotes protective Th1‐ and Th2‐mediated immunity to Leishmania majorinfection

Author

Pereira‐Manfro, Wânia F., Ribeiro‐Gomes, Flávia L., Filardy, Alessandra Almeida, Vellozo, Natália S., Guillermo, Landi V. C., Silva, Elisabeth M., Siegel, Richard M., DosReis, George A., and Lopes, Marcela F.

Abstract

T cell expression of caspase‐8 inhibitor vFLIP provides a Th1 cytokine environment, along with a protective Th2 response that increases immunity to Leishmania majorinfection. We investigated how apoptosis pathways mediated by death receptors and caspase‐8 affect cytokine responses and immunity to Leishmania majorparasites. Splenic CD4 T cells undergo activation‐induced apoptosis, and blockade of FasL‐Fas interaction increased IFN‐γ and IL‐4 cytokine responses to L. majorantigens. To block death receptor‐induced death, we used mice expressing a T cell‐restricted transgene for vFLIP. Inhibition of caspase‐8 activation in vFLIP mice enhanced Th1 and Th2 cytokine responses to L. majorinfection, even in the Th1‐prone B6 background. We also observed increased NO production by splenocytes from vFLIP mice upon T cell activation. Despite an exacerbated Th2 response, vFLIP mice controlled better L. majorinfection, with reduced lesions and lower parasite loads compared with WT mice. Moreover, injection of anti‐IL‐4 mAb in infected vFLIP mice disrupted control of parasite infection. Therefore, blockade of caspase‐8 activity in T cells improves immunity to L. majorinfection by promoting increased Th1 and Th2 responses.

Published
2014
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19. Myeloid‐derived suppressor cells help protective immunity to Leishmania majorinfection despite suppressed T cell responses

Author

Pereira, Wânia F., Ribeiro‐Gomes, Flávia L., Guillermo, Landi V. Costilla, Vellozo, Natália S., Montalvão, Fabrício, DosReis, George A., and Lopes, Marcela F.

Abstract

Infection with Leishmania majorelicits myeloid‐derived suppressor cells, which kill Leishmania parasites despite suppressed T‐cell proliferation. Th1/Th2 cytokines play a key role in immune responses to Leishmania majorby controlling macrophage activation for NO production and parasite killing. MDSCs, including myeloid precursors and immature monocytes, produce NO and suppress T cell responses in tumor immunity. We hypothesized that NO‐producing MDSCs could help immunity to L. majorinfection. Gr1hi(Ly6Chi) CD11bhiMDSCs elicited by L. majorinfection suppressed polyclonal and antigen‐specific T cell proliferation. Moreover, L. major‐induced MDSCs killed intracellular parasites in a NO‐dependent manner and reduced parasite burden in vivo. By contrast, treatment with ATRA, which induces MDSCs to differentiate into macrophages, increased development of lesions, parasite load, and T cell proliferation in draining LNs. Altogether, these results indicate that NO‐producing MDSCs help protective immunity to L. majorinfection, despite suppressed T cell proliferation.

Published
2011
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20. Interactions with apoptotic but not with necrotic neutrophils increase parasite burden in human macrophages infected with Leishmania amazonensis

Author

Afonso, Lilian, Borges, Valéria M., Cruz, Heloísa, Ribeiro‐Gomes, Flávia L., DosReis, George A., Dutra, Alberto Noronha, Clarêncio, Jorge, Oliveira, Camila I., Barral, Aldina, Barral‐Netto, Manoel, and Brodskyn, Cláudia I.

Abstract

Neutrophils are involved in the initial steps of most responses to pathogens. In the present study, we evaluated the effects of the interaction of apoptotic vs. necrotic human neutrophils on macrophage infection by Leishmania amazonensis. Phagocytosis of apoptotic, but not viable, neutrophils by Leishmania‐infected macrophages led to an increase in parasite burden via a mechanism dependent on TGF‐β1 and PGE2. Conversely, infected macrophages’ uptake of necrotic neutrophils induced killing of L. amazonensis. Leishmanicidal activity was dependent on TNF‐α and neutrophilic elastase. Nitric oxide was not involved in the killing of parasites, but the interaction of necrotic neutrophils with infected macrophages resulted in high superoxide production, a process reversed by catalase, an inhibitor of reactive oxygen intermediate production. Initial events after Leishmaniainfection involve interactions with neutrophils; we demonstrate that phagocytosis of these cells in an apoptotic or necrotic stage can influence the outcome of infection, driving either parasite survival or destruction.

Published
2008
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21. The Fas death pathway controls coordinated expansions of type 1 CD8 and type 2 CD4 T cells in Trypanosoma cruziinfection

Author

Guillermo, Landi V. Costilla, Silva, Elisabeth M., Ribeiro‐Gomes, Flávia L., De Meis, Juliana, Pereira, Wânia F., Yagita, Hideo, DosReis, George A., and Lopes, Marcela F.

Abstract

We investigated the role of the Fas ligand (FasL)/Fas death pathway on apoptosis and cytokine production by T cells in Trypanosoma cruziinfection. Anti‐FasL, but not anti‐TNF‐α or anti‐TRAIL, blocked activation‐induced cell death of CD8 T cells and increased secretion of IL‐10 and IL‐4 by CD4 T cells from T. cruzi‐infected mice. CD4 and CD8 T cells up‐regulated Fas/FasL expression during T. cruziinfection. However, Fas expression increased earlier in CD8 T cells, and a higher proportion of CD8 T cells was activated and expressed IFN‐γ compared with CD4 T cells. Injection of anti‐FasL in infected mice reduced parasitemia and CD8 T cell apoptosis and increased the ratio of CD8:CD4 T cells recovered from spleen and peritoneum. FasL blockade increased the number of activated T cells, enhanced NO production, and reduced parasite loads in peritoneal macrophages. Injection of anti‐FasL increased IFN‐γ secretion by splenocytes responding to T. cruziantigens but also exacerbated production of type 2 cytokines IL‐10 and IL‐4 at a late stage of acute infection. These results indicate that the FasL/Fas death pathway regulates apoptosis and coordinated cytokine responses by type 1 CD8 and type 2 CD4 T cells in T. cruziinfection.

Published
2007
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22. Macrophage interactions with neutrophils regulate Leishmania major infection.

Author

Ribeiro-Gomes FL, Otero AC, Gomes NA, Moniz-De-Souza MC, Cysne-Finkelstein L, Arnholdt AC, Calich VL, Coutinho SG, Lopes MF, and DosReis GA

Subjects
Animals, Cell Death immunology, Cells, Cultured, Coculture Techniques, Cytokines biosynthesis, Disease Susceptibility, Female, Genotype, Immunity, Innate, Leishmaniasis, Cutaneous genetics, Leishmaniasis, Cutaneous parasitology, Leishmaniasis, Cutaneous pathology, Leukocyte Elastase physiology, Macrophages, Peritoneal metabolism, Macrophages, Peritoneal parasitology, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred C57BL, Neutrophils enzymology, Neutrophils pathology, Neutrophils transplantation, Cell Communication immunology, Leishmania major growth & development, Leishmania major immunology, Leishmaniasis, Cutaneous immunology, Macrophages, Peritoneal immunology, Neutrophils immunology
Abstract

Macrophages are host cells for the pathogenic parasite Leishmania major. Neutrophils die and are ingested by macrophages in the tissues. We investigated the role of macrophage interactions with inflammatory neutrophils in control of L. major infection. Coculture of dead exudate neutrophils exacerbated parasite growth in infected macrophages from susceptible BALB, but killed intracellular L. major in resistant B6 mice. Coinjection of dead neutrophils amplified L. major replication in vivo in BALB, but prevented parasite growth in B6 mice. Neutrophil depletion reduced parasite load in infected BALB, but exacerbated infection in B6 mice. Exacerbated growth of L. major required PGE(2) and TGF-beta production by macrophages, while parasite killing depended on neutrophil elastase and TNF-alpha production. These results indicate that macrophage interactions with dead neutrophils play a previously unrecognized role in host responses to L. major infection.

Published
2004
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