4 results on '"Ester A, Mota"'
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2. Peripheral Organs of Dengue Fatal Cases Present Strong Pro-Inflammatory Response with Participation of IFN-Gamma-, TNF-Alpha- and RANTES-Producing Cells.
- Author
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Tiago F Póvoa, Edson R A Oliveira, Carlos A Basílio-de-Oliveira, Gerard J Nuovo, Vera L A Chagas, Natália G Salomão, Ada Maria de Barcelos Alves, Ester M Mota, and Marciano V Paes
- Subjects
Medicine ,Science - Abstract
Dengue disease is an acute viral illness caused by dengue virus (DENV) that can progress to hemorrhagic stages leading to about 20000 deaths every year worldwide. Despite many clinical investigations regarding dengue, the immunopathogenic process by which infected patients evolve to the severe forms is not fully understood. Apart from differences in virulence and the antibody cross reactivity that can potentially augment virus replication, imbalanced cellular immunity is also seen as a major concern in the establishment of severe dengue. In this context, the investigation of cellular immunity and its products in dengue fatal cases may provide valuable data to help revealing dengue immunopathogenesis. Here, based in four dengue fatal cases infected by the serotype 3 in Brazil, different peripheral organs (livers, lungs and kidneys) were studied to evaluate the presence of cell infiltrates and the patterns of local cytokine response. The overall scenario of the studied cases revealed a considerable systemic involvement of infection with mononuclear cells targeted to all of the evaluated organs, as measured by immunohistochemistry (IHC). Quantification of cytokine-expressing cells in peripheral tissues was also performed to characterize the ongoing inflammatory process by the severe stage of the disease. Increased levels of IFN-γ- and TNF-α-expressing cells in liver, lung and kidney samples of post-mortem subjects evidenced a strong pro-inflammatory induction in these tissues. The presence of increased RANTES-producing cell numbers in all analyzed organs suggested a possible link between the clinical status and altered vascular permeability. Co-staining of DENV RNA and IFN-γ or TNF-α using in situ hibridization and IHC confirmed the virus-specific trigger of the pro-inflammatory response. Taken together, this work provided additional evidences that corroborated with the traditional theories regarding the "cytokine storm" and the occurrence of uneven cellular immunity in response to DENV as major reasons for progress to severe disease.
- Published
- 2016
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3. Peripheral Organs of Dengue Fatal Cases Present Strong Pro-Inflammatory Response with Participation of IFN-Gamma-, TNF-Alpha- and RANTES-Producing Cells
- Author
-
Tiago F. Póvoa, Edson R. A. Oliveira, Carlos. A. Basílio-de-Oliveira, Gerard J. Nuovo, Vera L. A. Chagas, Natália G. Salomão, Ada Maria de Barcelos Alves, Ester M. Mota, and Marciano V. Paes
- Subjects
Male ,Viral Diseases ,Physiology ,lcsh:Medicine ,Kidney ,Dengue Fever ,Dengue ,White Blood Cells ,Animal Cells ,Immune Physiology ,Medicine and Health Sciences ,Lymphocytes ,lcsh:Science ,Chemokine CCL5 ,Lung ,Immunity, Cellular ,Innate Immune System ,Multidisciplinary ,T Cells ,Middle Aged ,Infectious Diseases ,Liver ,Cytokines ,Female ,Cellular Types ,Anatomy ,Research Article ,Neglected Tropical Diseases ,Adult ,Kupffer Cells ,Immune Cells ,Immunology ,Research and Analysis Methods ,Interferon-gamma ,Humans ,Immunohistochemistry Techniques ,Blood Cells ,Tumor Necrosis Factor-alpha ,Macrophages ,lcsh:R ,Correction ,Biology and Life Sciences ,Kidneys ,Cell Biology ,Renal System ,Molecular Development ,Tropical Diseases ,Histochemistry and Cytochemistry Techniques ,Immune System ,Immunologic Techniques ,lcsh:Q ,Developmental Biology - Abstract
Dengue disease is an acute viral illness caused by dengue virus (DENV) that can progress to hemorrhagic stages leading to about 20000 deaths every year worldwide. Despite many clinical investigations regarding dengue, the immunopathogenic process by which infected patients evolve to the severe forms is not fully understood. Apart from differences in virulence and the antibody cross reactivity that can potentially augment virus replication, imbalanced cellular immunity is also seen as a major concern in the establishment of severe dengue. In this context, the investigation of cellular immunity and its products in dengue fatal cases may provide valuable data to help revealing dengue immunopathogenesis. Here, based in four dengue fatal cases infected by the serotype 3 in Brazil, different peripheral organs (livers, lungs and kidneys) were studied to evaluate the presence of cell infiltrates and the patterns of local cytokine response. The overall scenario of the studied cases revealed a considerable systemic involvement of infection with mononuclear cells targeted to all of the evaluated organs, as measured by immunohistochemistry (IHC). Quantification of cytokine-expressing cells in peripheral tissues was also performed to characterize the ongoing inflammatory process by the severe stage of the disease. Increased levels of IFN-γ- and TNF-α-expressing cells in liver, lung and kidney samples of post-mortem subjects evidenced a strong pro-inflammatory induction in these tissues. The presence of increased RANTES-producing cell numbers in all analyzed organs suggested a possible link between the clinical status and altered vascular permeability. Co-staining of DENV RNA and IFN-γ or TNF-α using in situ hibridization and IHC confirmed the virus-specific trigger of the pro-inflammatory response. Taken together, this work provided additional evidences that corroborated with the traditional theories regarding the "cytokine storm" and the occurrence of uneven cellular immunity in response to DENV as major reasons for progress to severe disease.
- Published
- 2018
4. Peripheral Organs of Dengue Fatal Cases Present Strong Pro-Inflammatory Response with Participation of IFN-Gamma-, TNF-Alpha- and RANTES-Producing Cells
- Author
-
Gerard J. Nuovo, Natália Gedeão Salomão, Tiago F. Póvoa, Marciano Viana Paes, Ada M. B. Alves, Carlos Alberto Basílio-de-Oliveira, Vera Lucia Antunes Chagas, Edson R. A. Oliveira, and Ester Maria Mota
- Subjects
0301 basic medicine ,Cellular immunity ,Multidisciplinary ,lcsh:R ,lcsh:Medicine ,Kidney metabolism ,Biology ,Dengue virus ,medicine.disease ,medicine.disease_cause ,Virology ,Dengue fever ,03 medical and health sciences ,030104 developmental biology ,Immunity ,Immunology ,medicine ,biology.protein ,lcsh:Q ,Tumor necrosis factor alpha ,Antibody ,lcsh:Science ,Cytokine storm - Abstract
Dengue disease is an acute viral illness caused by dengue virus (DENV) that can progress to hemorrhagic stages leading to about 20000 deaths every year worldwide. Despite many clinical investigations regarding dengue, the immunopathogenic process by which infected patients evolve to the severe forms is not fully understood. Apart from differences in virulence and the antibody cross reactivity that can potentially augment virus replication, imbalanced cellular immunity is also seen as a major concern in the establishment of severe dengue. In this context, the investigation of cellular immunity and its products in dengue fatal cases may provide valuable data to help revealing dengue immunopathogenesis. Here, based in four dengue fatal cases infected by the serotype 3 in Brazil, different peripheral organs (livers, lungs and kidneys) were studied to evaluate the presence of cell infiltrates and the patterns of local cytokine response. The overall scenario of the studied cases revealed a considerable systemic involvement of infection with mononuclear cells targeted to all of the evaluated organs, as measured by immunohistochemistry (IHC). Quantification of cytokine-expressing cells in peripheral tissues was also performed to characterize the ongoing inflammatory process by the severe stage of the disease. Increased levels of IFN-γ- and TNF-α-expressing cells in liver, lung and kidney samples of post-mortem subjects evidenced a strong pro-inflammatory induction in these tissues. The presence of increased RANTES-producing cell numbers in all analyzed organs suggested a possible link between the clinical status and altered vascular permeability. Co-staining of DENV RNA and IFN-γ or TNF-α using in situ hibridization and IHC confirmed the virus-specific trigger of the pro-inflammatory response. Taken together, this work provided additional evidences that corroborated with the traditional theories regarding the "cytokine storm" and the occurrence of uneven cellular immunity in response to DENV as major reasons for progress to severe disease.
- Published
- 2016
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