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  1. Article ; Online: Upregulation of CD32 in T Cells from Infants with Severe Respiratory Syncytial Virus Disease: A New Costimulatory Pathway?

    Sananez, Inés / Raiden, Silvina / Holgado, María P / Seery, Vanesa / De Lillo, Leonardo / Davenport, Carolina / Ferrero, Fernando / Peeples, Mark E / Geffner, Jorge / Arruvito, Lourdes

    American journal of respiratory cell and molecular biology

    2020  Volume 63, Issue 1, Page(s) 133–136

    MeSH term(s) CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Female ; Humans ; Infant ; Male ; Receptors, IgG/metabolism ; Respiratory Syncytial Virus Infections/metabolism ; Respiratory Syncytial Viruses/pathogenicity ; Up-Regulation/physiology
    Chemical Substances Receptors, IgG
    Language English
    Publishing date 2020-06-30
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2020-0025LE
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Blood neutrophils from children with COVID-19 exhibit both inflammatory and anti-inflammatory markers.

    Seery, Vanesa / Raiden, Silvina C / Algieri, Silvia C / Grisolía, Nicolás A / Filippo, Daniela / De Carli, Norberto / Di Lalla, Sandra / Cairoli, Héctor / Chiolo, María J / Meregalli, Claudia N / Gimenez, Lorena I / Gregorio, Gabriela / Sarli, Mariam / Alcalde, Ana L / Davenport, Carolina / Bruera, María J / Simaz, Nancy / Pérez, Mariela F / Nivela, Valeria /
    Bayle, Carola / Tuccillo, Patricia / Agosta, María T / Pérez, Hernán / Villa Nova, Susana / Suárez, Patricia / Takata, Eugenia M / García, Mariela / Lattner, Jorge / Rolón, María J / Coll, Patricia / Sananez, Inés / Holgado, María P / Ferrero, Fernando / Geffner, Jorge / Arruvito, Lourdes

    EBioMedicine

    2021  Volume 67, Page(s) 103357

    Abstract: Background: Perhaps reflecting that children with COVID-19 rarely exhibit severe respiratory symptoms and often remain asymptomatic, little attention has been paid to explore the immune response in pediatric COVID-19. Here, we analyzed the phenotype and ...

    Abstract Background: Perhaps reflecting that children with COVID-19 rarely exhibit severe respiratory symptoms and often remain asymptomatic, little attention has been paid to explore the immune response in pediatric COVID-19. Here, we analyzed the phenotype and function of circulating neutrophils from children with COVID-19.
    Methods: An observational study including 182 children with COVID-19, 21 children with multisystem inflammatory syndrome (MIS-C), and 40 healthy children was performed in Buenos Aires, Argentina. Neutrophil phenotype was analyzed by flow cytometry in blood samples. Cytokine production, plasma levels of IgG antibodies directed to the spike protein of SARS-CoV-2 and citrullinated histone H3 were measured by ELISA. Cell-free DNA was quantified by fluorometry.
    Findings: Compared with healthy controls, neutrophils from children with COVID-19 showed a lower expression of CD11b, CD66b, and L-selectin but a higher expression of the activation markers HLA-DR, CD64 and PECAM-1 and the inhibitory receptors LAIR-1 and PD-L1. No differences in the production of cytokines and NETs were observed. Interestingly, the expression of CD64 in neutrophils and the serum concentration of IgG antibodies directed to the spike protein of SARS-CoV-2 distinguished asymptomatic from mild and moderate COVID-19.
    Interpretation: Acute lung injury is a prominent feature of severe COVID-19 in adults. A low expression of adhesion molecules together with a high expression of inhibitory receptors in neutrophils from children with COVID-19 might prevent tissue infiltration by neutrophils preserving lung function.
    Funding: This study was supported by the Ministry of Science and Technology (National Agency for Scientific and Technological Promotion, IP-COVID-19-0277 and PMO BID PICT 2018-2548), and University of Buenos Aires from Argentina (20020170100573BA).
    MeSH term(s) Antibodies, Viral/blood ; Argentina ; Biomarkers/blood ; COVID-19/blood ; COVID-19/immunology ; Case-Control Studies ; Child ; Child, Preschool ; Cytokines/blood ; Female ; Flow Cytometry ; Humans ; Immunoglobulin G/blood ; Infant ; Male ; Neutrophils/immunology ; SARS-CoV-2/immunology ; Spike Glycoprotein, Coronavirus/immunology ; Systemic Inflammatory Response Syndrome/blood ; Systemic Inflammatory Response Syndrome/immunology
    Chemical Substances Antibodies, Viral ; Biomarkers ; Cytokines ; Immunoglobulin G ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
    Language English
    Publishing date 2021-05-09
    Publishing country Netherlands
    Document type Journal Article ; Observational Study
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2021.103357
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Notch signaling proteins HES-1 and Hey-1 bind to insulin degrading enzyme (IDE) proximal promoter and repress its transcription and activity: Implications for cellular Aβ metabolism

    Leal, María C / Surace, Ezequiel I / Holgado, María P / Ferrari, Carina C / Tarelli, Rodolfo / Pitossi, Fernando / Wisniewski, Thomas / Castaño, Eduardo M / Morelli, Laura

    Biochimica et biophysica acta. Molecular cell research. 2012 Feb., v. 1823, no. 2

    2012  

    Abstract: Cerebral amyloid β (Aβ) accumulation is pathogenically associated with sporadic Alzheimer's disease (SAD). BACE-1 is involved in Aβ generation while insulin-degrading enzyme (IDE) partakes in Aβ proteolytic clearance. Vulnerable regions in AD brains show ...

    Abstract Cerebral amyloid β (Aβ) accumulation is pathogenically associated with sporadic Alzheimer's disease (SAD). BACE-1 is involved in Aβ generation while insulin-degrading enzyme (IDE) partakes in Aβ proteolytic clearance. Vulnerable regions in AD brains show increased BACE-1 protein levels and enzymatic activity while the opposite occurs with IDE. Another common feature in SAD brains is Notch1 overexpression. Here we demonstrate an increase in mRNA levels of Hey-1, a Notch target gene, and a decrease of IDE transcripts in the hippocampus of SAD brains as compared to controls. Transient transfection of Notch intracellular domain (NICD) in N2aSW cells, mouse neuroblastoma cells (N2a) stably expressing human amyloid precursor protein (APP) Swedish mutation, reduce IDE mRNA levels, promoting extracellular Aβ accumulation. Also, NICD, HES-1 and Hey-1 overexpression result in decreased IDE proximal promoter activity. This effect was mediated by 2 functional sites located at −379/−372 and −310−303 from the first translation start site in the −575/−19 (556bp) fragment of IDE proximal promoter. By site-directed mutagenesis of the IDE promoter region we reverted the inhibitory effect mediated by NICD transfection suggesting that these sites are indeed responsible for the Notch-mediated inhibition of the IDE gene expression. Intracranial injection of the Notch ligand JAG-1 in Tg2576 mice, expressing the Swedish mutation in human APP, induced overexpression of HES-1 and Hey-1 and reduction of IDE mRNA levels, respectively. Our results support our theory that a Notch-dependent IDE transcriptional modulation may impact on Aβ metabolism providing a functional link between Notch signaling and the amyloidogenic pathway in SAD.
    Keywords Alzheimer disease ; amyloid ; enzyme activity ; gene overexpression ; genes ; hippocampus ; humans ; insulin ; messenger RNA ; metabolism ; mice ; promoter regions ; proteolysis ; site-directed mutagenesis ; transcription (genetics) ; transfection
    Language English
    Dates of publication 2012-02
    Size p. 227-235.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 283444-3
    ISSN 0167-4889
    ISSN 0167-4889
    DOI 10.1016/j.bbamcr.2011.09.014
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: A poor and delayed anti-SARS-CoV2 IgG response is associated to severe COVID-19 in children.

    Sananez, Inés / Raiden, Silvina C / Algieri, Silvia C / Uranga, Macarena / Grisolía, Nicolás A / Filippo, Daniela / De Carli, Norberto / Lalla, Sandra Di / Cairoli, Héctor / Chiolo, María J / Meregalli, Claudia N / Cohen, Emilia / Mosquera, Graciela / Marcó Del Pont, María / Giménez, Lorena I / Gregorio, Gabriela / Sarli, Mariam / Alcalde, Ana L / Davenport, Carolina /
    Bruera, María J / Simaz, Nancy / Pérez, Mariela F / Nivela, Valeria / Bayle, Carola / Alvarez, Laura / Revetria, María / Tuccillo, Patricia / Agosta, María T / Pérez, Hernán / Nova, Susana Villa / Suárez, Patricia / Takata, Eugenia M / García, Mariela / Lattner, Jorge / Rolón, María J / Coll, Patricia / Salvatori, Melina / Piccardo, Claudio / Russo, Constanza / Varese, Augusto / Seery, Vanesa / Holgado, María P / Polo, María L / Ceballos, Ana / Nuñez, Myriam / Penedo, Juan Martín Gómez / Ferrero, Fernando / Geffner, Jorge / Arruvito, Lourdes

    EBioMedicine

    2021  Volume 72, Page(s) 103615

    Abstract: Background: Most children and youth develop mild or asymptomatic disease during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, a very small number of patients suffer severe Coronavirus induced disease 2019 (COVID-19). ... ...

    Abstract Background: Most children and youth develop mild or asymptomatic disease during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, a very small number of patients suffer severe Coronavirus induced disease 2019 (COVID-19). The reasons underlying these different outcomes remain unknown.
    Methods: We analyzed three different cohorts: children with acute infection (n=550), convalescent children (n=138), and MIS-C (multisystem inflammatory syndrome in children, n=42). IgG and IgM antibodies to the spike protein of SARS-CoV-2, serum-neutralizing activity, plasma cytokine levels, and the frequency of circulating Follicular T helper cells (cTfh) and plasmablasts were analyzed by conventional methods.
    Findings: Fifty-eight percent of the children in the acute phase of infection had no detectable antibodies at the time of sampling while a seronegative status was found in 25% and 12% of convalescent and MIS-C children, respectively. When children in the acute phase of the infection were stratified according disease severity, we found that contrasting with the response of children with asymptomatic, mild and moderate disease, children with severe COVID-19 did not develop any detectable response. A defective antibody response was also observed in the convalescent cohort for children with severe disease at the time of admission. This poor antibody response was associated to both, a low frequency of cTfh and a high plasma concentration of inflammatory cytokines.
    Interpretation: A weak and delayed kinetic of antibody response to SARS-CoV-2 together with a systemic pro-inflammatory profile characterize pediatric severe COVID-19. Because comorbidities are highly prevalent in children with severe COVID-19, further studies are needed to clarify their contribution in the weak antibody response observed in severe disease.
    Funding: National Agency for Scientific and Technological Promotion from Argentina (IP-COVID-19-0277 and PMO-BID-PICT2018-2548).
    MeSH term(s) Antibodies, Viral/blood ; Antibody Formation ; Argentina ; COVID-19/blood ; COVID-19/complications ; COVID-19/immunology ; Child ; Child, Preschool ; Cytokines/blood ; Female ; Humans ; Immunoglobulin G/blood ; Immunoglobulin M/blood ; Infant ; Male ; SARS-CoV-2/immunology ; Systemic Inflammatory Response Syndrome/blood ; Systemic Inflammatory Response Syndrome/immunology
    Chemical Substances Antibodies, Viral ; Cytokines ; Immunoglobulin G ; Immunoglobulin M
    Language English
    Publishing date 2021-10-11
    Publishing country Netherlands
    Document type Journal Article ; Observational Study
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2021.103615
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Notch signaling proteins HES-1 and Hey-1 bind to insulin degrading enzyme (IDE) proximal promoter and repress its transcription and activity: implications for cellular Aβ metabolism.

    Leal, María C / Surace, Ezequiel I / Holgado, María P / Ferrari, Carina C / Tarelli, Rodolfo / Pitossi, Fernando / Wisniewski, Thomas / Castaño, Eduardo M / Morelli, Laura

    Biochimica et biophysica acta

    2011  Volume 1823, Issue 2, Page(s) 227–235

    Abstract: Cerebral amyloid β (Aβ) accumulation is pathogenically associated with sporadic Alzheimer's disease (SAD). BACE-1 is involved in Aβ generation while insulin-degrading enzyme (IDE) partakes in Aβ proteolytic clearance. Vulnerable regions in AD brains show ...

    Abstract Cerebral amyloid β (Aβ) accumulation is pathogenically associated with sporadic Alzheimer's disease (SAD). BACE-1 is involved in Aβ generation while insulin-degrading enzyme (IDE) partakes in Aβ proteolytic clearance. Vulnerable regions in AD brains show increased BACE-1 protein levels and enzymatic activity while the opposite occurs with IDE. Another common feature in SAD brains is Notch1 overexpression. Here we demonstrate an increase in mRNA levels of Hey-1, a Notch target gene, and a decrease of IDE transcripts in the hippocampus of SAD brains as compared to controls. Transient transfection of Notch intracellular domain (NICD) in N2aSW cells, mouse neuroblastoma cells (N2a) stably expressing human amyloid precursor protein (APP) Swedish mutation, reduce IDE mRNA levels, promoting extracellular Aβ accumulation. Also, NICD, HES-1 and Hey-1 overexpression result in decreased IDE proximal promoter activity. This effect was mediated by 2 functional sites located at -379/-372 and -310-303 from the first translation start site in the -575/-19 (556 bp) fragment of IDE proximal promoter. By site-directed mutagenesis of the IDE promoter region we reverted the inhibitory effect mediated by NICD transfection suggesting that these sites are indeed responsible for the Notch-mediated inhibition of the IDE gene expression. Intracranial injection of the Notch ligand JAG-1 in Tg2576 mice, expressing the Swedish mutation in human APP, induced overexpression of HES-1 and Hey-1 and reduction of IDE mRNA levels, respectively. Our results support our theory that a Notch-dependent IDE transcriptional modulation may impact on Aβ metabolism providing a functional link between Notch signaling and the amyloidogenic pathway in SAD.
    MeSH term(s) Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Aspartic Acid Endopeptidases/metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line ; Hippocampus/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Insulysin/genetics ; Insulysin/metabolism ; Mice ; Promoter Regions, Genetic ; Protein Binding ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction/physiology ; Transcription Factor HES-1 ; Transcription, Genetic
    Chemical Substances Amyloid beta-Protein Precursor ; Basic Helix-Loop-Helix Transcription Factors ; Cell Cycle Proteins ; HEY1 protein, human ; Homeodomain Proteins ; Receptors, Notch ; Transcription Factor HES-1 ; HES1 protein, human (149348-15-2) ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; BACE1 protein, human (EC 3.4.23.46) ; Insulysin (EC 3.4.24.56)
    Language English
    Publishing date 2011-10-19
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2011.09.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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