MARIA IRMA SEIXAS DUARTE
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/06 - Laboratório de Imunopatologia da Esquistossomose e outras Parasitoses, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/06 - Laboratório de Imunopatologia da Esquistossomose e outras Parasitoses, Hospital das Clínicas, Faculdade de Medicina - Líder
78 resultados
Resultados de Busca
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- Esophageal mucosa in HIV infection: A ""deeper"" look at this little spoken organ(2017) WERNECK-SILVA, Ana Luiza; PAGLIARI, Carla; PATZINA, Roseli A.; TAKAKURA, Cleusa Fumica Hirata; DUARTE, Maria IrmaBackground and Aim: Although the esophagus is a common site of opportunistic infection in AIDS patients, little is known about the impact of HIV as well as opportunistic infection in the esophageal mucosa. Our aim is to analyze the esophageal immune profile in HIV+ patients with different immunological status with and without the opportunistic Candida infection. Methods: Immunohistochemistry to CD4+ and CD8+ T-cells, gamma-interferon, transforming growth factor-beta, interleukin (IL)-4, IL-6, IL-13, and IL-17 was performed in esophageal samples of 40 chronically HIV+ patients under highly active antiretroviral therapy (16 with Candida esophagitis, 12 virologically non-supressed with blood CD4 count < 500, and 12 virologically suppressed with blood CD4 count > 500; the latter two groups without esophageal candidiasis). The controls were 12 HIV-negative healthy individuals. Results: Esophageal CD4+ T-cell expression in HIV+ patients did not differ from the control group (P = 0.50). Mucosal CD8+ T-cell expression was significantly increased in HIV+ patients (P = 0.0018). Candida esophagitis and virologically non-supressed HIV+ patients with CD4 < 500 showed an increased expression of IL-17 and IL-6 with fewer expressions of gamma-interferon, more attenuated in the latter group. Transforming growth factor-beta was increased only in virologically suppressed HIV+ patients with CD4 > 500. IL-4 and IL-13 were similar to the control group. Conclusion: In contrast to CD8+ T-cell expression, esophageal CD4+ T-cell expression does not reflect the HIV+ patient's immunological status. T-helper 17 (Th17) response seems to play a role in the esophageal mucosa of virologically non-supressed HIV+ patients with blood CD4 < 500. Candida esophagitis showed a Th1/ Th17 response but seems to be dominantly regulated by the Th17 pathway.
- Analysis of microvasculature phenotype and endothelial activation markers in skin lesions of lacaziosis (Lobomycosis)(2015) QUARESMA, Juarez A. S.; BRITO, Maysa V.; SOUSA, Jorge R.; SILVA, Luciana M.; HIRAI, Kelly E.; ARAUJO, Rafael S.; BRITO, Arival C. de; CARNEIRO, Francisca R. O.; FUZII, Hellen T.; PAGLIARI, Carla; SOTTO, Mirian N.; DUARTE, Maria I. S.Jorge Lobo's disease is a rare mycosis characterized by chronic inflammation, which causes skin lesions in the absence of visceral dissemination. The disease occurs mainly in hot and humid climates and most cases have been registered in the Brazilian Amazon region. This study investigated possible microvascular alterations in skin lesions caused by infection with Lacazia loboi which may interfere with the clinical progression of the disease. Immunohistochemistry was used to evaluate the density of blood and lymphatic vessels, as well as expression of the cell adhesion molecules ICAM-1, VCAM-1 and E-selectin. The results showed a reduced number of blood (62.66 +/- 20.30 vessels/mm(2)) and lymphatic vessels (3.55 +/- 5.84 vessels/mm(2)) in Jorge Lobo's disease when compared to control skin (169.66 +/- 66.38 blood vessels/mm(2) and 8 +/- 2.17 lymphatic vessels/mm(2)). There were a larger number of vessels expressing ICAM-1 (27.58 +/- 15.32 vessels/mm(2)) and VCAM-1 (7.55 +/- 6.2 vessels/mm(2)). No difference was observed in the expression of E-selectin (4.66 +/- 11 vessels/mm(2)). Taken together, the results indicate changes in the local microvasculature which may interfere with the development of an efficient cell-mediated immune response and may explain restriction of the fungus to the site of injury.
- M2-Polarized Macrophages Determine Human Cutaneous Lesions in Lacaziosis(2020) BARBOZA, Tania Cristina; SOTTO, Mirian Nacagami; KANASHIRO-GALO, Luciane; BRITO, Arival Cardoso de; DUARTE, Maria Irma Seixas; QUARESMA, Juarez Antonio Simoes; PAGLIARI, CarlaLacaziosis is a cutaneous chronic mycosis caused by Lacazia loboi. Macrophages are important cells in the host immune response in fungal infections. The macrophage population exhibits strong plasticity that varies according to the stimuli in the microenvironment of lesions M1 profile promotes a Th1 pattern of cytokines and a microbicidal function and M2 is related to Th2 cytokines and immunomodulatory response. We investigated the population of M1 and M2 polarized macrophages in human cutaneous lesions. A total of 27 biopsies from human lesions were submitted to an immunohistochemistry protocol using antibodies to detect M1 and M2 macrophages (Arginase-1, CD163, iNOS, RBP-J and cMAF). We could observe high number of cells expressing Arginase1, CD163 and c-MAF that correspond to elements of the M2 profile of macrophage, over iNOS and RBP-J (elements of the M1 profile). The results suggest a predominant phenotype of M2 macrophages, which have an immunomodulatory role and probably contributing to chronicity of Lacaziosis.
- Severe Leptospirosis Features in the Spleen Indicate Cellular Immunosuppression Similar to That Found in Septic Shock(2019) DUARTE-NETO, Amaro Nunes; CRODA, Julio; PAGLIARI, Carla; SORIANO, Francisco Garcia; NICODEMO, Antonio Carlos; DUARTE, Maria Irma SeixasObjectives: To compare microscopic and immunologic features in the spleens of patients who died of pulmonary hemorrhage and shock caused by leptospirosis (11 cases) or Gram-positive/-negative bacterial septic shock (10 cases) to those from control spleens (12 cases from splenectomy). Methodology: Histological features in the red pulp and white pulp were analyzed using archived samples by a semi quantitative score. Immunohistochemistry was used for the recognition of immune cell markers, cytokines, caspase-3 and Leptospira antigens. Results: The control group differed significantly from the leptospirosis and septic shock patients which demonstrate strong similarities: diffuse congestion in the red pulp with a moderate to intense infiltration of plasma cells and polymorphonuclear cells; follicles with marked atrophy; high density of CD20(+) cells; low density of NK, TCD4(+) and active caspase-3 positive cells and strong expression of IL-10; leptospirosis patients had higher S100 and TNF-alpha positive cells in the spleen than the other groups. Conclusion: The results suggest that an immunosuppressive state develops at the terminal stage of severe leptospirosis with pulmonary hemorrhage and shock similar to that of patients with septic shock, with diffuse endothelial activation in the spleen, splenitis, and signs of disturbance in the innate and adaptive immunity in the spleen. The presence of leptospiral antigens in 73% of the spleens of the leptospirosis patients suggests the etiological agent contributes directly to the pathogenesis of the lesions. Our results support therapeutic approaches involving antibiotic and immunomodulatory treatments for leptospirosis patients and suggest that leptospirosis patients, which are usually young men with no co-morbidities, form a good group for studying sepsis and septic shock.
- New Insights into the Mechanism of Immune-Mediated Tissue Injury in Yellow Fever: The Role of Immunopathological and Endothelial Alterations in the Human Lung Parenchyma(2022) VASCONCELOS, Danielle Barbosa; FALCAO, Luiz Fabio Magno; PONTE, Lucas Coutinho Tuma Da; SILVA, Camilla Costa; MARTINS, Livia Caricio; NUNES, Bruno Tardelli Diniz; MARTINS FILHO, Arnaldo Jorge; FRANCO, Edna Cristina Santos; DUARTE, Maria Irma Seixas; SOUSA, Jorge Rodrigues De; VASCONCELOS, Pedro Fernando Da Costa; QUARESMA, Juarez Antonio SimoesYellow fever (YF) may cause lesions in different organs. There are no studies regarding the in situ immune response in the human lung and investigating immunopathological aspects in fatal cases can help to better understand the evolution of the infection. Lung tissue samples were collected from 10 fatal cases of human yellow fever and three flavivirus-negative controls who died of other causes and whose lung parenchymal architecture was preserved. In YFV-positive fatal cases, the main histopathological changes included the massive presence of diffuse alveolar inflammatory infiltrate, in addition to congestion and severe hemorrhage. The immunohistochemical analysis of tissues in the lung parenchyma showed significantly higher expression of E-selectin, P-selectin, ICAM-1, VCAM-1 in addition to cytokines such as IL-4, IL-10, IL-13, TNF- alpha, IFN-gamma and TGF-beta compared to the negative control. The increase in immunoglobulins ICAM-1 and VCAM-1 results in strengthening of tissue transmigration signaling. E-selectin and P-selectin actively participate in this process of cell migration and formation of the inflammatory infiltrate. IFN-gamma and TNF-alpha participate in the process of cell injury and viral clearance. The cytokines IL-4 and TGF-beta, acting in synergism, participate in the process of tissue regeneration and breakdown. The anti-inflammatory cytokines IL-4, IL-10 and IL-13 also act in the reduction of inflammation and tissue repair. Our study indicates that the activation of the endothelium aggravates the inflammatory response by inducing the expression of adhesion molecules and cytokines that contribute to the rolling, recruitment, migration and eliciting of the inflammatory process in the lung parenchyma, contributing to the fatal outcome of the disease.
- Tegumentary leishmaniasis mimicking visceralization in a cirrhotic patient: atypical cutaneous lesions and local immunological features(2020) VERNAL, Sebastian; CASAL, Yuri; VIEIRA, Lucas T.; AMATO, Valdir S.; DUARTE, Maria Irma S.; NASTRI, Ana Catharina S. S.Tegumentary leislunaniasis (TL) diagnosis is challenging due to the lack of a gold standard diagnostic tool. The diagnosis is significantly harder in regions where visceral leishmaniasis (VL) is also prevalent since immunological tests may present cross-reactivity. A cirrhotic patient from an endemic Brazilian region for TL and VL presented with atypical cutaneous lesions, a usual clinico-laboratory feature of VL (including a positive rk39 test result), but he was diagnosed with TL histopathologically; VL was ruled out by necropsy. Physicians working in co-prevalent areas should be aware of atypical features, unusual clinical course, and unexpected laboratory findings of leishmaniasis.
- Endothelium Activation during Severe Yellow Fever Triggers an Intense Cytokine-Mediated Inflammatory Response in the Liver Parenchyma(2022) OLIMPIO, Fabio Alves; FALCAO, Luiz Fabio Magno; CARVALHO, Marcos Luiz Gaia; LOPES, Jeferson da Costa; MENDES, Caio Cesar Henriques; FILHO, Arnaldo Jorge Martins; SILVA, Carlos Augusto Moreira da; MIRANDA, Vanessa do Socorro Cabral; SANTOS, Lais Carneiro dos; VILACOERT, Fellipe Souza da Silva; CRUZ, Ana Cecilia Ribeiro; GALUCIO, Vanessa Costa Alves; AZEVEDO, Raimunda do Socorro da Silva; MARTINS, Livia Caricio; DUARTE, Maria Irma Seixas; SOUSA, Jorge Rodrigues de; VASCONCELOS, Pedro Fernando da Costa; QUARESMA, Juarez Antonio SimoesYellow fever (YF) is a pansystemic disease caused by the yellow fever virus (YFV), the prototype species of the family Flaviviridae and genus Flavivirus, and has a highly complex host-pathogen relationship, in which endothelial dysfunction reflects viral disease tropism. In this study, the in situ endothelial response was evaluated. Liver tissue samples were collected from 21 YFV-positive patients who died due to the disease and five flavivirus-negative controls who died of other causes and whose hepatic parenchyma architecture was preserved. Immunohistochemical analysis of tissues in the hepatic parenchyma of YF cases showed significantly higher expression of E-selectin, P-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and very late antigen-4 in YFV-positive cases than in flavivirus-negative controls. These results indicate that endothelium activation aggravates the inflammatory response by inducing the expression of adhesion molecules that contribute to the rolling, recruitment, migration, and construction of the inflammatory process in the hepatic parenchyma in fatal YF cases.
conferenceObject The Role of the Social Worker Concerning Intestinal Rehabilitation and Transplantation in a Latin American Center(2021) GALVAO, F.; LEE, A.; TANJI, J.; RANA, T.; DUARTE, M.; SCABIA, T.; WAISBERG, D.; ROCHA, M.; PINHEIRO, R.; CARNEIRO-D'ALBUQUERQUE, L.- In situ apoptosis of adaptive immune cells and the cellular escape of rabies virus in CNS from patients with human rabies transmitted by Desmodus rotundus(2011) FERNANDES, Elaine Raniero; ANDRADE JR., Heitor Franco de; LANCELLOTTI, Carmen Lucia Penteado; QUARESMA, Juarez Antonio Simoes; DEMACHKI, Samia; VASCONCELOS, Pedro Fernando da Costa; DUARTE, Maria Irma SeixasThe aim of the current study was to investigate the apoptosis of neurons, astrocytes and immune cells from human patients that were infected with rabies virus by vampire bats bite. Apoptotic neurons were identified by their morphology and immune cells were identified using double immunostaining. There were very few apoptotic neurons present in infected tissue samples, but there was an increase of apoptotic infiltrating CD4+ and TCD8+ adaptive immune cells in the rabies infected tissue. No apoptosis was present in NK, macrophage and astrocytes. The dissemination of the human rabies virus within an infected host may be mediated by viral escape of the virus from an infected cell and may involve an anti-apoptotic mechanism, which does not kill the neuron or pro-apoptosis of TCD4+ and TCD8+ lymphocytes and which allows for increased proliferation of the virus within the CNS by attenuation of the adaptive immune response.
- Role of Th17 Cytokines in the Liver's Immune Response during Fatal Yellow Fever: Triggering Cell Damage Mechanisms(2022) CARVALHO, Marcos Luiz Gaia; FALCAO, Luiz Fabio Magno; LOPES, Jeferson da Costa; MENDES, Caio Cesar Henriques; OLIMPIO, Fabio Alves; MIRANDA, Vanessa do Socorro Cabral; SANTOS, Lais Carneiro dos; MORAES, Daniel Dias Pinheiro de; BERTONSIN FILHO, Marcos Virgilio; COSTA, Luccas Delgado da; AZEVEDO, Raimunda do Socorro da Silva; CRUZ, Ana Cecilia Ribeiro; GALUCIO, Vanessa Costa Alves; MARTINS, Livia Caricio; DUARTE, Maria Irma Seixas; MARTINS FILHO, Arnaldo Jorge; SOUSA, Jorge Rodrigues de; VASCONCELOS, Pedro Fernando da Costa; QUARESMA, Juarez Antonio SimoesYellow fever (YF) is an infectious and acute viral haemorrhagic disease that triggers a cascade of host immune responses. We investigated the Th17 cytokine profile in the liver tissue of patients with fatal YF. Liver tissue samples were collected from 26 deceased patients, including 21 YF-positive and 5 flavivirus-negative patients, with preserved hepatic parenchyma architecture, who died of other causes. Histopathological and immunohistochemical analysis were performed on the liver samples to evaluate the Th17 profiles (ROR-gamma, STAT3, IL-6, TGF-beta, IL-17A, and IL-23). Substantial differences were found in the expression levels of these markers between the patients with fatal YF and controls. A predominant expression of Th17 cytokine markers was observed in the midzonal region of the YF cases, the most affected area in the liver acinus, compared with the controls. Histopathological changes in the hepatic parenchyma revealed cellular damage characterised mainly by the presence of inflammatory cell infiltrates, Councilman bodies (apoptotic cells), micro/macrovesicular steatosis, and lytic and coagulative necrosis. Hence, Th17 cytokines play a pivotal role in the immunopathogenesis of YF and contribute markedly to triggering cell damage in patients with fatal disease outcomes.