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5 results on '"Luz P. Quebrada Palacio"'

1. Circulating T Follicular Helper Cell Abnormalities Associated to Different Clinical Forms of Chronic Chagas Disease

Author

Luz P. Quebrada Palacio, Esteban R. Fernández, Yolanda Hernández-Vásquez, Patricia B. Petray, and Miriam Postan

Subjects
T follicular helper cells, circulating Tfh subsets, CXCR3, CCR6, Human Chagas disease, Trypanosoma cruzi, Microbiology, QR1-502
Abstract

Multiple perturbations of the immune response affecting a range of cells have been reported in Trypanosoma cruzi-infected individuals and associated to clinical manifestations of chronic Chagas disease. There is a paucity of knowledge about the role of T follicular helper (Tfh) cells in this infection. Here, we sought to characterize circulating Tfh (cTfh) cells in chronic Chagas disease patients and to identify potential associations with disease severity in humans. cTfh cells were characterized by flow cytometry in freshly isolated PBMCs from 7 T. cruzi-infected asymptomatic patients (ASYMP), 5 patients with chronic chagasic dilated cardiomyopathy (CCC) and 8 healthy controls, using antibodies against chemokine receptors CXCR5, CXCR3, CCR6, and CCR7. Our results showed significant expansion of CD4+CD45RO+CXCR5+CCR6+ cells in ASYMP and CCC patients, along with a contraction of CD4+CD45RO+CXCR5+CXCR3-CCR6- (cTfh2) cells. ASYMP patients further exhibited decreased CD4+CD45RO+CXCR5+CXCR3+CCR6- (cTfh1) cells and expanded CD4+CD45RO+CXCR5+CXCR3-CCR6+ (cTfh17) cells while CCC patients exhibited significantly increased frequencies of CD4+CD45RO+CXCR5+CCR7+ cells. Linear regression analysis revealed a positive trend of CD4+CD45RO+CXCR5+CXCR3+CCR6+ (cTfh1/17) cells and negative trends of cTfh1 and cTfh2 cells as disease was more severe. There was no correlation between the frequencies of cTfh cells and circulating CD19+IgD-IgG+ cells or serum levels of T. cruzi-specific IgG. These results demonstrate that the cTfh compartment of humans chronically infected with T. cruzi comprises expanded CCR6-expressing cells and reduced cTfh2 cells. The association of discrete phenotypic changes in cTfh subsets with different clinical forms suggests the potential contribution of T follicular helper cells to Chagas heart disease progression.

Published
2020
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2. Altered distribution of peripheral blood memory B cells in humans chronically infected with Trypanosoma cruzi.

Author

Esteban R Fernández, Gabriela C Olivera, Luz P Quebrada Palacio, Mariela N González, Yolanda Hernandez-Vasquez, Natalia María Sirena, María L Morán, Oscar S Ledesma Patiño, and Miriam Postan

Subjects
Medicine, Science
Abstract

Numerous abnormalities of the peripheral blood T cell compartment have been reported in human chronic Trypanosoma cruzi infection and related to prolonged antigenic stimulation by persisting parasites. Herein, we measured circulating lymphocytes of various phenotypes based on the differential expression of CD19, CD4, CD27, CD10, IgD, IgM, IgG and CD138 in a total of 48 T. cruzi-infected individuals and 24 healthy controls. Infected individuals had decreased frequencies of CD19+CD27+ cells, which positively correlated with the frequencies of CD4+CD27+ cells. The contraction of CD19+CD27+ cells was comprised of IgG+IgD-, IgM+IgD- and isotype switched IgM-IgD- memory B cells, CD19+CD10+CD27+ B cell precursors and terminally differentiated CD19+CD27+CD138+ plasma cells. Conversely, infected individuals had increased proportions of CD19+IgG+CD27-IgD- memory and CD19+IgM+CD27-IgD+ transitional/naïve B cells. These observations prompted us to assess soluble CD27, a molecule generated by the cleavage of membrane-bound CD27 and used to monitor systemic immune activation. Elevated levels of serum soluble CD27 were observed in infected individuals with Chagas cardiomyopathy, indicating its potentiality as an immunological marker for disease progression in endemic areas. In conclusion, our results demonstrate that chronic T. cruzi infection alters the distribution of various peripheral blood B cell subsets, probably related to the CD4+ T cell deregulation process provoked by the parasite in humans.

Published
2014
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3. Circulating T Follicular Helper Cell Abnormalities Associated to Different Clinical Forms of Chronic Chagas Disease

Author

Luz P. Quebrada Palacio, Esteban R. Fernández, Yolanda Hernández-Vásquez, Patricia B. Petray, and Miriam Postan

Subjects
0301 basic medicine, Microbiology (medical), CD4-Positive T-Lymphocytes, Receptors, CXCR5, T Follicular Helper Cells, Trypanosoma cruzi, 030106 microbiology, Immunology, lcsh:QR1-502, T FOLLICULAR HELPER CELLS, C-C chemokine receptor type 7, chemical and pharmacologic phenomena, C-C chemokine receptor type 6, CXCR3, Microbiology, lcsh:Microbiology, CXCR5, CD19, Flow cytometry, 03 medical and health sciences, purl.org/becyt/ford/3.3 [https], Immune system, Cellular and Infection Microbiology, immune system diseases, Medicine, Humans, Chagas Disease, HUMAN CHAGAS DISEASE, medicine.diagnostic_test, biology, business.industry, hemic and immune systems, TRYPANOSOMA CRUZI, T-Lymphocytes, Helper-Inducer, Brief Research Report, Human Chagas disease, 030104 developmental biology, Infectious Diseases, CIRCULATING TFH SUBSETS, biology.protein, purl.org/becyt/ford/3 [https], circulating Tfh subsets, Antibody, business, CCR6
Abstract

Multiple perturbations of the immune response affecting a range of cells have been reported in Trypanosoma cruzi-infected individuals and associated to clinical manifestations of chronic Chagas disease. There is a paucity of knowledge about the role of T follicular helper (Tfh) cells in this infection. Here, we sought to characterize circulating Tfh (cTfh) cells in chronic Chagas disease patients and to identify potential associations with disease severity in humans. cTfh cells were characterized by flow cytometry in freshly isolated PBMCs from 7 T. cruzi-infected asymptomatic patients (ASYMP), 5 patients with chronic chagasic dilated cardiomyopathy (CCC) and 8 healthy controls, using antibodies against chemokine receptors CXCR5, CXCR3, CCR6, and CCR7. Our results showed significant expansion of CD4+CD45RO+CXCR5+CCR6+ cells in ASYMP and CCC patients, along with a contraction of CD4+CD45RO+CXCR5+CXCR3-CCR6- (cTfh2) cells. ASYMP patients further exhibited decreased CD4+CD45RO+CXCR5+CXCR3+CCR6- (cTfh1) cells and expanded CD4+CD45RO+CXCR5+CXCR3-CCR6+ (cTfh17) cells while CCC patients exhibited significantly increased frequencies of CD4+CD45RO+CXCR5+CCR7+ cells. Linear regression analysis revealed a positive trend of CD4+CD45RO+CXCR5+CXCR3+CCR6+ (cTfh1/17) cells and negative trends of cTfh1 and cTfh2 cells as disease was more severe. There was no correlation between the frequencies of cTfh cells and circulating CD19+IgD-IgG+ cells or serum levels of T. cruzi-specific IgG. These results demonstrate that the cTfh compartment of humans chronically infected with T. cruzi comprises expanded CCR6-expressing cells and reduced cTfh2 cells. The association of discrete phenotypic changes in cTfh subsets with different clinical forms suggests the potential contribution of T follicular helper cells to Chagas heart disease progression. Fil: Quebrada Palacio, Luz Piedad. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina Fil: Fernández, Esteban Rodrigo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina Fil: Hernandez Vasquez, Yolanda Maria. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina Fil: Petray, Patricia Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones en Microbiología y Parasitología Médica. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones en Microbiología y Parasitología Médica; Argentina Fil: Postan, Miriam. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán". Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben"; Argentina

Published
2019

4. Monocyte glycolysis determines CD8+ T cell functionality in human Chagas disease

Author

Yolanda Hernandez-Vasquez, Laura Morelli, Miriam Postan, Eugenio Antonio Carrera Silva, Natalia Eberhardt, Luz P. Quebrada Palacio, Maria Pilar Aoki, Gastón Bergero, Laura Marina Visconti, Angel Ramón Minguez, Pamela V. Martino Adami, and Liliana Maria Sanmarco

Subjects
Male, 0301 basic medicine, Protozoan Proteins, Cell Communication, CD8-Positive T-Lymphocytes, Lymphocyte Activation, Monocytes, Glycolysis Inhibition, 0302 clinical medicine, Chlorocebus aethiops, Cytotoxic T cell, Chemistry, purl.org/becyt/ford/3.1 [https], General Medicine, Middle Aged, Medicina Básica, medicine.anatomical_structure, 030220 oncology & carcinogenesis, purl.org/becyt/ford/3 [https], Female, GLICOLISIS, Glycolysis, Research Article, Adult, Chagas disease, CIENCIAS MÉDICAS Y DE LA SALUD, MACROFAGOS, Trypanosoma cruzi, T cell, Primary Cell Culture, Inmunología, Nitric Oxide, Sudden death, Peripheral blood mononuclear cell, Young Adult, 03 medical and health sciences, medicine, Animals, Humans, Chagas Disease, Vero Cells, Monocyte, medicine.disease, Coculture Techniques, Oxidative Stress, 030104 developmental biology, Case-Control Studies, Immunology, Tyrosine, TRIPANOZOMA CRUZI, CD8
Abstract

Chagas disease is a life-long pathology resulting from Trypanosoma cruzi infection. It represents one of the most frequent causes of heart failure and sudden death in Latin America. Herein we provide evidence that aerobic glycolytic pathway activation in monocytes drives nitric oxide (NO) production, triggering tyrosine nitration (TN) on CD8 T cells and dysfunction in patients with chronic Chagas disease. Monocytes from patients exhibited higher frequency of hypoxia inducible factor (HIF)-1α and increased expression of its target genes/proteins. Non-classical monocytes are expanded in patients´ peripheral blood and represent an important source of NO. Monocytes entail CD8 T cell surface nitration since both the frequency of non-classical monocytes and that of NO-producing monocytes, positively correlated with the percentage of TN+ lymphocytes. Inhibition of glycolysis in (in vitro) infected peripheral blood mononuclear cells decreased the inflammatory properties of monocytes/macrophages diminishing the frequency of IL-1β- and NO-producing cells. In agreement, glycolysis inhibition reduced the percentage of TN+CD8 T cells improving their functionality. Altogether, these results clearly evidence that glycolysis governs oxidative stress on monocytes and modulates monocyte-T cell interplay in human chronic Chagas disease. Understanding the pathological immune mechanisms that sustains inflammatory environment in human pathology is key to design improved therapies. Fil: Sanmarco, Liliana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Eberhardt, Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Bergero, Gastón. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Quebrada Palacio, Luz Piedad. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán". Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben"; Argentina Fil: Martino Adami, Pamela Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Visconti, Laura Marina. Hospital Nuestra Señora de la Misericordia; Argentina Fil: Minguez, Angel Ramón. Hospital Nuestra Señora de la Misericordia; Argentina Fil: Hernández-Vasquez, Yolanda. Instituto Nacional de Parasitologia Mario Fatala Chaben; Argentina Fil: Carrera Silva, Eugenio Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Morelli, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Postan, Miriam. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán". Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben"; Argentina Fil: Aoki, Maria del Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina

Published
2019
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5. Phenotypic diversity and drug susceptibility of Trypanosoma cruzi TcV clinical isolates

Author

Adriana Parodi-Talice, Jacqueline Búa, Alina Elizabeth Perrone, Luz P. Quebrada Palacio, Miriam Postan, Yolanda Hernandez-Vasquez, Mariela N. González, Quebrada Palacio L.P., González M.N., Hernandez-Vasquez Y., Perrone A.E., Parodi Tálice Adriana Magdalena, Universidad de la República (Uruguay). Facultad de Ciencias. Instituto de Biología, Bua J., and Postan M.

Subjects
0301 basic medicine, Chagas disease, Adult, Male, Genotype, Trypanosoma cruzi, 030231 tropical medicine, Argentina, Drug Resistance, Protozoan Proteins, lcsh:Medicine, Parasitemia, Biology, Microbiology, Ciencias Biológicas, purl.org/becyt/ford/1 [https], 03 medical and health sciences, Mice, 0302 clinical medicine, Biología Celular, Microbiología, Phenotypic diversity, Chlorocebus aethiops, medicine, Animals, Humans, Chagas Disease, Nifurtimox, Amastigote, lcsh:Science, purl.org/becyt/ford/1.6 [https], Vero Cells, Multidisciplinary, lcsh:R, Middle Aged, medicine.disease, biology.organism_classification, Trypanocidal Agents, 030104 developmental biology, Phenotype, Benznidazole, Female, lcsh:Q, Congenital transmission, Trypanosomiasis, CIENCIAS NATURALES Y EXACTAS, medicine.drug, Pentamidine
Abstract

Trypanosoma cruzi is a genetically heterogeneous group of organisms that cause Chagas disease. It has been long suspected that the clinical outcome of the disease and response to therapeutic agents are, at least in part, related to the genetic characteristics of the parasite. Herein, we sought to validate the significance of the genotype of T. cruzi isolates recovered from patients with different clinical forms of Chagas disease living in Argentina on their biological behaviour and susceptibility to drugs. Genotype identification of the newly established isolates confirmed the reported predominance of TcV, with a minor frequency of TcI. Epimastigote sensitivity assays demonstrated marked dissimilar responses to benznidazole, nifurtimox, pentamidine and dihydroartemisinin in vitro. Two TcV isolates exhibiting divergent response to benznidazole in epimastigote assays were further tested for the expression of anti-oxidant proteins. Benznidazole-resistant BOL-FC10A epimastigotes had decreased expression of Old Yellow Enzyme and cytosolic superoxide dismutase, and over-expression of mitochondrial superoxide dismutase and tryparedoxin- 1, compared to benznidazole-susceptible AR-SE23C parasites. Drug sensitivity assays on intracellular amastigotes and trypomastigotes reproduced the higher susceptibility of AR-SE23C over BOL-FC10A parasites to benznidazole observed in epimastigotes assays. However, the susceptibility/resistance profile of amastigotes and trypomastigotes to nifurtimox, pentamidine and dihydroartemisinin varied markedly with respect to that of epimastigotes. C3H/He mice infected with AR-SE23C trypomastigotes had higher levels of parasitemia and mortality rate during the acute phase of infection compared to mice infected with BOL-FC10A trypomastigotes. Treatment of infected mice with benznidazole or nifurtimox was efficient to reduce patent parasitemia induced by either isolate. Nevertheless, qPCR performed at 70 dpi revealed parasite DNA in the blood of mice infected with AR-SE23C but not in BOL-FC10A infected mice. These results demonstrate high level of intra-type diversity which may represent an important obstacle for the testing of chemotherapeutic agents. Fil: Quebrada Palacio, Luz Piedad. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: González, Mariela Natacha. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Hernandez Vasquez, Yolanda Maria. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina Fil: Perrone, Alina Elizabeth. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Parodi Talice, Adriana. Universidad de la República; Uruguay Fil: Bua, Jacqueline Elena. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Postan, Miriam. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina

Published
2018
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