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21 results on '"Cortes, Paulo R."'

1. Phylogenetic analysis and comparative genomics of SARS-CoV-2 from survivor and non-survivor COVID-19 patients in Cordoba, Argentina

Author

Olivero, Nadia B., Gonzalez-Reiche, Ana S., Re, Viviana E., Castro, Gonzalo M., Pisano, María B., Sicilia, Paola, Barbas, María G., Khan, Zenab, van de Guchte, Adriana, Dutta, Jayeeta, Cortes, Paulo R., Hernandez-Morfa, Mirelys, Zappia, Victoria E., Ortiz, Lucia, Geiger, Ginger, Rajao, Daniela, Perez, Daniel R., van Bakel, Harm, and Echenique, Jose

Published
2022
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2. Intracellular Streptococcus pneumoniae develops enhanced fluoroquinolone persistence during influenza A coinfection.

Author

Hernandez-Morfa, Mirelys, Reinoso-Vizcaino, Nicolas M., Zappia, Victoria E., Olivero, Nadia B., Cortes, Paulo R., Stempin, Cinthia C., Perez, Daniel R., and Echenique, Jose

Subjects
STREPTOCOCCUS pneumoniae, STREPTOCOCCAL diseases, INFLUENZA, PNEUMOCOCCAL pneumonia, VIRUS diseases, MIXED infections, OXIDATIVE stress
Abstract

Streptococcus pneumoniae is a major pathogen responsible for severe complications in patients with prior influenza A virus (IAV) infection. We have previously demonstrated that S. pneumoniae exhibits increased intracellular survival within IAV-infected cells. Fluoroquinolones (FQs) are widely used to treat pneumococcal infections. However, our prior work has shown that S. pneumoniae can develop intracellular FQ persistence, a phenomenon triggered by oxidative stress within host cells. This persistence allows the bacteria to withstand high FQ concentrations. In this study, we show that IAV infection enhances pneumococcal FQ persistence during intracellular survival within pneumocytes, macrophages, and neutrophils. This enhancement is partly due to increased oxidative stress induced by the viral infection. We find that this phenotype is particularly pronounced in autophagy-proficient host cells, potentially resulting from IAV-induced blockage of autophagosome-lysosome fusion. Moreover, we identified several S. pneumoniae genes involved in oxidative stress response that contribute to FQ persistence, including sodA (superoxide dismutase), clpL (chaperone), nrdH (glutaredoxin), and psaB (Mn+2 transporter component). Our findings reveal a novel mechanism of antibiotic persistence promoted by viral infection within host cells. This underscores the importance of considering this phenomenon when using FQs to treat pneumococcal infections, especially in patients with concurrent influenza A infection. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Different evolution of S. aureus methicillin-resistant and methicillin-susceptible infections, Argentina

Author

Barcudi, Danilo, primary, Blasko, Enrique, additional, Gonzalez, María José, additional, Gagetti, Paula, additional, Lamberghini, Ricardo, additional, Garnero, Analía, additional, Sarkis, Claudia, additional, Faccone, Diego, additional, Lucero, Celeste, additional, Tosoroni, Dario, additional, Bocco, José L., additional, Corso, Alejandra, additional, Sola, Claudia, additional, Borda de Notario, Noemí, additional, Bermejo, Joaquín, additional, Farfan, Silvia Mariela, additional, Herrera, Patricia Carrizo, additional, Pallone, Elida, additional, Neumann, Gabriela, additional, Almuzara, Marisa N., additional, Dinerstein, Edith, additional, Gañete, Marcelo, additional, Togneri, Ana María, additional, Andres, Patricia, additional, Madsen, Elizabeth, additional, Aguila, Damian, additional, Perez, Jorgelina F., additional, Marchiaro, Patricia, additional, Orellana, Nora, additional, Castillo, Marcelo del, additional, Baroni, Maria Rosa, additional, Ezcurra, Gustavo Cesar, additional, Amalfi y Olivia Gear, Flavia, additional, Pereira, Nancy N., additional, Occello, María T., additional, García, Guillermo R., additional, Villegas, Josefina M., additional, Nizzo, Jorge Gonzalez, additional, Toffoli, Marcelo, additional, Granados, Gabriela, additional, Miranda, Maria R., additional, Pato, Ana M., additional, Achinelli, Fernando, additional, Almada, Gladys Margarita, additional, Sanchez, Ana Laura, additional, Gouts, Nuria Martina, additional, Vargas, Marcela, additional, Vega, Edgar Adan, additional, Vázquez, Cinthia, additional, Cano, Hortensia, additional, Cech, Norma Esther, additional, Rodriguez, Sergio, additional, Montanaro, Patricia, additional, Paredes, Marisa, additional, Garnero, Analía V., additional, Vilches, Viviana, additional, Quiros, Rodolfo, additional, Cané, Alejandro, additional, Uranga, Macarena, additional, González, Liliana, additional, Sanchez, Maria Lucrecia, additional, Tirao, Eugenia, additional, Machain, Mónica, additional, Fleitas, Hugo, additional, Blanca Mena, Norma Cudmani, additional, Lacono, Marisa Alejandra, additional, Núñez, María R., additional, Schinchirimini, María Martha, additional, Abate, Héctor, additional, García, Beatriz, additional, Benvenutti, María Luz, additional, Giordano, Laura, additional, Daniel Morales, Juan Carlos, additional, Vescina, Cecilia, additional, Di Bella, Adriana, additional, Taponier, Gabriela, additional, Daciuk, Lucia, additional, Degregoris, Gabriela, additional, Marianelli, Leonardo, additional, Lopez, Teresa, additional, Martins, Marcelo, additional, Wolff, Lidia, additional, Amador, Silvia G., additional, Segovia, Carina Evangelina, additional, Camisassa, Lilia, additional, Sosa, Luciana, additional, Flores, Sonia, additional, Rombola, Eduardo, additional, Gasparotto, Ana M., additional, Carrizo, Valeria Ocaña, additional, Greco, Carlos Quinteros, additional, Ballari, Estefania, additional, Minoli, Maria J., additional, Garutti, Alicia, additional, Cuniberti, Valentina, additional, Díaz, Elda, additional, Ciarlantini, Marcos, additional, Gonzalez, José, additional, Herrero, Ivana Lis, additional, Ocampo, Ivana, additional, Lopez, Adriana, additional, Cortes, Paulo R., additional, González, Patricia, additional, Calvari, Miriam, additional, Piersigilli, Andrea, additional, Maria Bilbao, Liliana Ether, additional, Blanco, Facundo, additional, Decca, Laura, additional, Fernando Riera, Claudio Manchado, additional, Beccereca, Graciela, additional, Vega, Daniela, additional, Canigia, Liliana Fernández, additional, Freuler, Cristina, additional, Della Latta, María Paula, additional, Mayer-Wolf, Micaela, additional, Yahni, Diego, additional, Smayevsky, Jorgelina, additional, Scocozza, Laura, additional, Diaz, María Susana, additional, Benegas, Liliana, additional, Pryluka, Daniel, additional, Manganello, Silvana, additional, Costa, Rosana, additional, Moyano, Mónica, additional, Zintgraff, Jonathan, additional, Garcia, Fabiana, additional, Figueroa, Miriam, additional, Landa, Mariana, additional, Bernardi, German, additional, Minguez, Angel, additional, Arriero, Graciela Alicia, additional, Díaz, María Silvia, additional, Mudrik, Maria Gabriela, additional, Panini, Nancy Veronica, additional, Cuello, Alejandra, additional, Gonzalez, Cristina Alicia, additional, Gerlach, Erica, additional, Kuo, Lein Hung, additional, Sparo, Mónica Delfina, additional, Gentile, Jorge Hector, additional, Henández, Claudia, additional, Ernst, Adriana Margarita, additional, Ensinck, Gabriela, additional, Alfonso, Claudia María, additional, Rodriguez Brieschke, Maria Teresa, additional, D´Alessandro, Daniela, additional, Vivaldo, María Silvana, additional, Malianni, Belen, additional, Berejnoi, Ana, additional, Falco, Adriana, additional, Andriani, María Ester, additional, Fernandez, Silvana, additional, Contreras, Karina, additional, Quiroga, Adriana, additional, Stafforini, Graciela María, additional, Aparicio, Maria Cristina, additional, Hernández, Claudia, additional, Pereda, Rosana, additional, Echave, Cecilia, additional, Arrieta, Maria Fernanda, additional, Musa, Daniela, additional, Zaloff Dakoff, Ana Maria, additional, and Corallo, Teresa Alicia, additional

Published
2023
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7. Additional file 4 of Phylogenetic analysis and comparative genomics of SARS-CoV-2 from survivor and non-survivor COVID-19 patients in Cordoba, Argentina

Author

Olivero, Nadia B., Gonzalez-Reiche, Ana S., Re, Viviana E., Castro, Gonzalo M., Pisano, María B., Sicilia, Paola, Barbas, María G., Khan, Zenab, van de Guchte, Adriana, Dutta, Jayeeta, Cortes, Paulo R., Hernandez-Morfa, Mirelys, Zappia, Victoria E., Ortiz, Lucia, Geiger, Ginger, Rajao, Daniela, Perez, Daniel R., van Bakel, Harm, and Echenique, Jose

Subjects
Data_FILES
Abstract

Additional file 4: Table S3.

Published
2022
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8. Additional file 2 of Phylogenetic analysis and comparative genomics of SARS-CoV-2 from survivor and non-survivor COVID-19 patients in Cordoba, Argentina

Author

Olivero, Nadia B., Gonzalez-Reiche, Ana S., Re, Viviana E., Castro, Gonzalo M., Pisano, María B., Sicilia, Paola, Barbas, María G., Khan, Zenab, van de Guchte, Adriana, Dutta, Jayeeta, Cortes, Paulo R., Hernandez-Morfa, Mirelys, Zappia, Victoria E., Ortiz, Lucia, Geiger, Ginger, Rajao, Daniela, Perez, Daniel R., van Bakel, Harm, and Echenique, Jose

Subjects
Data_FILES
Abstract

Additional file 2: Table S1.

Published
2022
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9. Acidic stress induces autolysis by a CSP-independent ComE pathway in Streptococcus pneumoniae

Author

Pinas, German E., Cortes, Paulo R., Orio, Andrea G. Albarracin, and Echenique, Jose

Subjects
Streptococcus pneumoniae -- Physiological aspects, Peptides -- Physiological aspects, Biological sciences
Abstract

In Streptococcus pneumoniae, autolysis is considered a programmed cell-death process executed principally by the major autolysin (LytA), and the underlying mechanism causing its activation is not completely understood. It is known that autolysis is triggered by competence development at alkaline pH and regulated by a two-component system, ComDE, which senses a competence-stimulating peptide (CSP) and behaves as a quorum-sensing mechanism. In this work, we found that acidic stress triggered a LytA-mediated autolysis and, curiously, this phenomenon was regulated by a CSP-independent ComE pathway. A further analysis of a hyperactive ComD mutant revealed that ComE needs to be phosphorylated to activate acidic stress-induced lysis (ASIL). The comE transcripts were induced by acidic culture conditions, suggesting that ComE could be sensing acidic stress. We also investigated CiaRH, a two-component system whose null mutants show a comE derepression and a CSP-dependent autolysis induction at alkaline pH. By analysis of cia comE double mutants, we demonstrated that CiaRH protected cells from ASIL by a ComE-independent pathway. Here, we propose that Come is the principal route of the signalling pathway that determines a global stress response, and clearly regulates the induction of the LytA-mediated programmed cell death in S. pneumoniae. Acidic stress may represent for S. pneumoniae an alternative condition, in addition to competence and antibiotics, to assure the release of virulence factors, DNA and cell-wall compounds by autolysis, favouring genetic exchange and contributing to its pathogenesis.

Published
2008

10. The pneumococcal two-component system SirRH is linked to enhanced intracellular survival of Streptococcus pneumoniae in influenza-infected pulmonary cells

Author

Reinoso-Vizcaíno, Nicolás M., primary, Cian, Melina B., additional, Cortes, Paulo R., additional, Olivero, Nadia B., additional, Hernandez-Morfa, Mirelys, additional, Piñas, Germán E., additional, Badapanda, Chandan, additional, Rathore, Ankita, additional, Perez, Daniel R., additional, and Echenique, José, additional

Published
2020
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13. The pneumococcal two-component system VisRH is linked to enhanced intracellular survival ofStreptococcus pneumoniaein influenza-infected pneumocytes

Author

Reinoso-Vizcaíno, Nicolás M., primary, Cian, Melina B., additional, Cortes, Paulo R., additional, Olivero, Nadia B., additional, Hernandez-Morfa, Mirelys, additional, Piñas, Germán E., additional, Badapanda, Chandan, additional, Rathore, Ankita, additional, Perez, Daniel R., additional, and Echenique, José, additional

Published
2019
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14. Crosstalk between the serine/threonine kinase StkP and the response regulator ComE controls the stress response and intracellular survival of Streptococcus pneumoniae

Author

Piñas, Germán E., primary, Reinoso-Vizcaino, Nicolás M., additional, Yandar Barahona, Nubia Y., additional, Cortes, Paulo R., additional, Duran, Rosario, additional, Badapanda, Chandan, additional, Rathore, Ankita, additional, Bichara, Dario R., additional, Cian, Melina B., additional, Olivero, Nadia B., additional, Perez, Daniel R., additional, and Echenique, José, additional

Published
2018
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21. Characterization of In Vitro-Generated and Clinical Optochin-Resistant Strains of Streptococcus pneumoniaeIsolated from Argentina

Author

Cortes, Paulo R., Orio, Andrea G. Albarraci´n, Regueira, Mabel, as, and Echenique, Jose´

Abstract

ABSTRACTOptochin susceptibility is a key test used for pneumococcal diagnosis, but optochin-resistant (Optr) pneumococci have been reported in the last 2 decades. In this work, we characterized eight Optrclinical strains which presented a new mutation, G47V, a predominant A49S mutation (recently reported in Brazil) and A49T. These mutations were found in the csubunit of the F0F1ATPase encoded by the atpCgene, and W206C was found in the asubunit encoded by the atpAgene. The Optrclinical isolates were analyzed by BOX PCR, multilocus sequence typing, and serotype and antimicrobial resistance profiles, and they showed no epidemiological relationship. To characterize the Optrmutations that could emerge among clinical strains, we studied a pool of spontaneous Optrcolonies obtained in vitro from the virulent D39 strain. We compared the atpACmutations of these Optrpneumococci (with or without passage through C57BL/6 mice) with those described in the clinical isolates. This analysis revealed three new mutations, G47V and L26M in the csubunit and L184S in the asubunit. Most of the mutations identified in the laboratory-generated Optrstrains were also found in clinical strains, with the exception of the L26M and L184S mutations, and we suppose that both mutations could emerge among invasive strains in the future. Considering that atpACare essential genes, we propose that all spontaneous mutations that confer in vitro optochin resistance would not present severe physiological alterations in S. pneumoniaeand may be carried by circulating pneumococcal strains.

Published
2008
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