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  1. Article: Akt Inhibition Promotes Autophagy and Clearance of Group B

    Pantazi, Ioanna / Papafragkos, Iosif / Kolliniati, Ourania / Lapi, Ioanna / Tsatsanis, Christos / Vergadi, Eleni

    Pathogens (Basel, Switzerland)

    2022  Volume 11, Issue 10

    Abstract: ... Group ... ...

    Abstract Group B
    Language English
    Publishing date 2022-09-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens11101134
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: SARS-CoV-2 modulates inflammatory responses of alveolar epithelial type II cells

    Al-Qahtani, Ahmed A / Pantazi, Ioanna / Alhamlan, Fatimah S / Alothaid, Hani / Matou-Nasri, Sabine / Sourvinos, George / Vergadi, Eleni / Tsatsanis, Christos

    Frontiers in immunology

    2022  Volume 13, Page(s) 1020624

    Abstract: Background: SARS-CoV-2 infects through the respiratory route and triggers inflammatory response by affecting multiple cell types including type II alveolar epithelial cells. SARS-CoV-2 triggers signals : Aim: Aim of the present study was to ... ...

    Abstract Background: SARS-CoV-2 infects through the respiratory route and triggers inflammatory response by affecting multiple cell types including type II alveolar epithelial cells. SARS-CoV-2 triggers signals
    Aim: Aim of the present study was to investigate the effect of SARS-CoV2 on type II alveolar epithelial cells, focusing on signals initiated by its S protein and their impact on the expression of inflammatory mediators.
    Results: For this purpose A549 alveolar type II epithelial cells were exposed to SARS CoV2 S recombinant protein and the expression of inflammatory mediators was measured. The results showed that SARS-CoV-2 S protein decreased the expression and secretion of IL8, IL6 and TNFα, 6 hours following stimulation, while it had no effect on IFNα, CXCL5 and PAI-1 expression. We further examined whether SARS-CoV-2 S protein, when combined with TLR2 signals, which are also triggered by SARS-CoV2 and its envelope protein, exerts a different effect in type II alveolar epithelial cells. Simultaneous treatment of A549 cells with SARS-CoV-2 S protein and the TLR2 ligand PAM3csk4 decreased secretion of IL8, IL6 and TNFα, while it significantly increased IFNα, CXCL5 and PAI-1 mRNA expression. To investigate the molecular pathway through which SARS-CoV-2 S protein exerted this immunomodulatory action in alveolar epithelial cells, we measured the induction of MAPK/ERK and PI3K/AKT pathways and found that SARS-CoV-2 S protein induced the activation of the serine threonine kinase AKT. Treatment with the Akt inhibitor MK-2206, abolished the inhibitory effect of SARS-CoV-2 S protein on IL8, IL6 and TNFα expression, suggesting that SARS-CoV-2 S protein mediated its action
    Conclusion: The findings of our study, showed that SARS-CoV-2 S protein suppressed inflammatory responses in alveolar epithelial type II cells at early stages of infection through activation of the PI3K/AKT pathway. Thus, our results suggest that at early stages SARS-CoV-2 S protein signals inhibit immune responses to the virus allowing it to propagate the infection while in combination with TLR2 signals enhances PAI-1 expression, potentially affecting the local coagulation cascade.
    MeSH term(s) Humans ; Alveolar Epithelial Cells/metabolism ; SARS-CoV-2 ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt ; Tumor Necrosis Factor-alpha ; RNA, Viral ; Plasminogen Activator Inhibitor 1 ; Interleukin-6 ; Interleukin-8 ; Toll-Like Receptor 2 ; COVID-19
    Chemical Substances spike protein, SARS-CoV-2 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Tumor Necrosis Factor-alpha ; RNA, Viral ; Plasminogen Activator Inhibitor 1 ; Interleukin-6 ; Interleukin-8 ; Toll-Like Receptor 2
    Language English
    Publishing date 2022-10-31
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.1020624
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: SARS-CoV-2/ACE2 Interaction Suppresses IRAK-M Expression and Promotes Pro-Inflammatory Cytokine Production in Macrophages.

    Pantazi, Ioanna / Al-Qahtani, Ahmed A / Alhamlan, Fatimah S / Alothaid, Hani / Matou-Nasri, Sabine / Sourvinos, George / Vergadi, Eleni / Tsatsanis, Christos

    Frontiers in immunology

    2021  Volume 12, Page(s) 683800

    Abstract: The major cause of death in SARS-CoV-2 infected patients is due to de-regulation of the innate immune system and development of cytokine storm. SARS-CoV-2 infects multiple cell types in the lung, including macrophages, by engagement of its spike (S) ... ...

    Abstract The major cause of death in SARS-CoV-2 infected patients is due to de-regulation of the innate immune system and development of cytokine storm. SARS-CoV-2 infects multiple cell types in the lung, including macrophages, by engagement of its spike (S) protein on angiotensin converting enzyme 2 (ACE2) receptor. ACE2 receptor initiates signals in macrophages that modulate their activation, including production of cytokines and chemokines. IL-1R-associated kinase (IRAK)-M is a central regulator of inflammatory responses regulating the magnitude of TLR responsiveness. Aim of the work was to investigate whether SARS-CoV-2 S protein-initiated signals modulate pro-inflammatory cytokine production in macrophages. For this purpose, we treated PMA-differentiated THP-1 human macrophages with SARS-CoV-2 S protein and measured the induction of inflammatory mediators including IL6, TNFα, IL8, CXCL5, and MIP1a. The results showed that SARS-CoV-2 S protein induced IL6, MIP1a and TNFα mRNA expression, while it had no effect on IL8 and CXCL5 mRNA levels. We further examined whether SARS-CoV-2 S protein altered the responsiveness of macrophages to TLR signals. Treatment of LPS-activated macrophages with SARS-CoV-2 S protein augmented IL6 and MIP1a mRNA, an effect that was evident at the protein level only for IL6. Similarly, treatment of PAM3csk4 stimulated macrophages with SARS-CoV-2 S protein resulted in increased mRNA of IL6, while TNFα and MIP1a were unaffected. The results were confirmed in primary human peripheral monocytic cells (PBMCs) and isolated CD14+ monocytes. Macrophage responsiveness to TLR ligands is regulated by IRAK-M, an inactive IRAK kinase isoform. Indeed, we found that SARS-CoV-2 S protein suppressed IRAK-M mRNA and protein expression both in THP1 macrophages and primary human PBMCs and CD14+ monocytes. Engagement of SARS-CoV-2 S protein with ACE2 results in internalization of ACE2 and suppression of its activity. Activation of ACE2 has been previously shown to induce anti-inflammatory responses in macrophages. Treatment of macrophages with the ACE2 activator DIZE suppressed the pro-inflammatory action of SARS-CoV-2. Our results demonstrated that SARS-CoV-2/ACE2 interaction rendered macrophages hyper-responsive to TLR signals, suppressed IRAK-M and promoted pro-inflammatory cytokine expression. Thus, activation of ACE2 may be a potential anti-inflammatory therapeutic strategy to eliminate the development of cytokine storm observed in COVID-19 patients.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Angiotensin-Converting Enzyme 2/metabolism ; COVID-19/immunology ; Cytokine Release Syndrome/immunology ; Gene Expression Regulation ; Humans ; Immunity, Innate ; Inflammation Mediators/metabolism ; Interleukin-1 Receptor-Associated Kinases/genetics ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Lipopolysaccharides/immunology ; Macrophages/immunology ; Macrophages/virology ; Protein Binding ; SARS-CoV-2/physiology ; Spike Glycoprotein, Coronavirus/metabolism ; THP-1 Cells ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Inflammation Mediators ; Interleukin-6 ; Lipopolysaccharides ; MAPKAP1 protein, human ; Spike Glycoprotein, Coronavirus ; Tumor Necrosis Factor-alpha ; spike protein, SARS-CoV-2 ; IRAK3 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Language English
    Publishing date 2021-06-23
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.683800
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Emotional Stroop interference for threatening words is related to reduced EEG δ-β coupling and low attentional control.

    Putman, Peter / Arias-Garcia, Elsa / Pantazi, Ioanna / van Schie, Charlotte

    International journal of psychophysiology : official journal of the International Organization of Psychophysiology

    2012  Volume 84, Issue 2, Page(s) 194–200

    Abstract: Previously, electroencephalographic (EEG) delta-beta coupling (positive correlation between power in the fast beta and slow delta frequency bands) has been related to affective processing. For instance, differences in delta-beta coupling have been ... ...

    Abstract Previously, electroencephalographic (EEG) delta-beta coupling (positive correlation between power in the fast beta and slow delta frequency bands) has been related to affective processing. For instance, differences in delta-beta coupling have been observed between people in a psychological stress condition and controls. We previously reported relationships between attentional threat processing and delta-beta coupling and individual differences in attentional control. The present study extended and replicated these findings in a large mixed gender sample (N=80). Results demonstrated that emotional Stroop task interference for threatening words was related to self-reported attentional inhibition capacity and frontal delta-beta coupling. There was no clear gender difference for delta-beta coupling (only a non-significant trend) and the relationship between delta-beta coupling and attentional threat-processing was not affected by gender. These results replicate and extend an earlier finding concerning delta-beta coupling and cognitive affect regulation and further clarify relationships between delta-beta coupling, attentional control, and threat-processing.
    MeSH term(s) Adolescent ; Adult ; Attention/physiology ; Delta Rhythm/physiology ; Electroencephalography/methods ; Emotions/physiology ; Female ; Humans ; Male ; Stroop Test ; Young Adult
    Language English
    Publishing date 2012-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605645-3
    ISSN 1872-7697 ; 0167-8760
    ISSN (online) 1872-7697
    ISSN 0167-8760
    DOI 10.1016/j.ijpsycho.2012.02.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1925: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: EEG theta/beta ratio as a potential biomarker for attentional control and resilience against deleterious effects of stress on attention.

    Putman, Peter / Verkuil, Bart / Arias-Garcia, Elsa / Pantazi, Ioanna / van Schie, Charlotte

    Cognitive, affective & behavioral neuroscience

    2013  Volume 14, Issue 2, Page(s) 782–791

    Abstract: Anxious stress compromises cognitive executive performance. This occurs, for instance, in cognitive performance anxiety (CPA), in which anxiety about one's cognitive performance causes that performance to actually deteriorate (e.g., test anxiety). This ... ...

    Abstract Anxious stress compromises cognitive executive performance. This occurs, for instance, in cognitive performance anxiety (CPA), in which anxiety about one's cognitive performance causes that performance to actually deteriorate (e.g., test anxiety). This is thought to result from a prefrontal cortically (PFC) mediated failure of top-down attentional control over stress-induced automatic processing of threat-related information. In addition, stress-induced increased catecholamine influx into the PFC may directly compromise attentional function. Previous research has suggested that the ratio between resting state electroencephalographic (EEG) low- and high-frequency power (the theta/beta ratio) is related to trait attentional control, which might moderate these effects of stress on attentional function. The goals of the present study were to test the novel prediction that theta/beta ratio moderates the deleterious effects of CPA-like anxious stress on state attentional control and to replicate a previous finding that the theta/beta ratio is related to self-reported trait attentional control. After recording of baseline frontal EEG signals, 77 participants performed a stress induction or a control procedure. Trait attentional control was assessed with the Attentional Control Scale, whereas stress-induced changes in attentional control and anxiety were measured with self-report visual analogue scales. The hypothesized moderating influence of theta/beta ratio on the effects of stress on state attentional control was confirmed. Theta/beta ratio explained 28% of the variance in stress-induced deterioration of self-reported attentional control. The negative relationship between theta/beta ratio and trait attentional control was replicated (r = -.33). The theta/beta ratio reflects, likely prefrontally mediated, attentional control, and should be a useful biomarker for the study of CPA and other anxiety-cognition interactions.
    MeSH term(s) Adolescent ; Analysis of Variance ; Attention Deficit Disorder with Hyperactivity/etiology ; Attention Deficit Disorder with Hyperactivity/pathology ; Beta Rhythm/physiology ; Biomarkers ; Electroencephalography ; Female ; Humans ; Male ; Prefrontal Cortex/physiopathology ; Psychiatric Status Rating Scales ; Stress, Psychological/complications ; Theta Rhythm/physiology ; Young Adult
    Chemical Substances Biomarkers
    Language English
    Publishing date 2013-11-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2029088-3
    ISSN 1531-135X ; 1530-7026
    ISSN (online) 1531-135X
    ISSN 1530-7026
    DOI 10.3758/s13415-013-0238-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5947: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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