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  1. Article ; Online: Wnt/β-Catenin Protects Lymphocytes from HIV-Mediated Apoptosis via Induction of Bcl-xL.

    Albalawi, Yasmeen A / Narasipura, Srinivas D / Al-Harthi, Lena

    Viruses

    2022  Volume 14, Issue 7

    Abstract: HIV infection mediates the apoptosis of lymphocytes, the mechanism of which is multifaceted. Here, we evaluated the role of Wnt/β-catenin signaling in HIV-associated T cell apoptosis, as Wnt/β-catenin regulates the transcriptional activity of genes ... ...

    Abstract HIV infection mediates the apoptosis of lymphocytes, the mechanism of which is multifaceted. Here, we evaluated the role of Wnt/β-catenin signaling in HIV-associated T cell apoptosis, as Wnt/β-catenin regulates the transcriptional activity of genes impacting apoptosis. We specifically investigated the role of the Wnt/β-catenin pathway in the HIV-associated apoptosis of CD4+ T cells and CD4dimCD8bright T cells, a population that is infected by HIV. We found that the induction of β-catenin, via a 6-bromoindirubin-3-oxime (BIO), significantly rescued HIV-infected CD4+ and CD4dimCD8bright T cells from apoptosis by >40−50%. Further, a small-molecule inhibitor of the Wnt/β-catenin pathway (PNU-74654) reversed BIO-mediated protection from HIV-associated apoptosis. BIO also induced Bcl-xL, an anti-apoptotic protein, and a target gene of Wnt/β-catenin, in CD4+ and CD4dimCD8bright T cells by approximately 3-fold. Inhibiting Bcl-xL by WEHI-539 abrogated β-catenin-mediated apoptotic protection in infected CD4+ and CD4dimCD8bright T cells. Collectively, these findings demonstrate that engaging Wnt/β-catenin signaling in HIV-infected T cells protects them from HIV-associated apoptosis by inducing Bcl-xL.
    MeSH term(s) Apoptosis ; CD4-Positive T-Lymphocytes/metabolism ; HIV Infections ; Humans ; Wnt Signaling Pathway ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances beta Catenin
    Language English
    Publishing date 2022-07-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v14071469
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Wnt/β-Catenin Protects Lymphocytes from HIV-Mediated Apoptosis via Induction of Bcl-xL

    Albalawi, Yasmeen A. / Narasipura, Srinivas D. / Al-Harthi, Lena

    Viruses. 2022 July 02, v. 14, no. 7

    2022  

    Abstract: HIV infection mediates the apoptosis of lymphocytes, the mechanism of which is multifaceted. Here, we evaluated the role of Wnt/β-catenin signaling in HIV-associated T cell apoptosis, as Wnt/β-catenin regulates the transcriptional activity of genes ... ...

    Abstract HIV infection mediates the apoptosis of lymphocytes, the mechanism of which is multifaceted. Here, we evaluated the role of Wnt/β-catenin signaling in HIV-associated T cell apoptosis, as Wnt/β-catenin regulates the transcriptional activity of genes impacting apoptosis. We specifically investigated the role of the Wnt/β-catenin pathway in the HIV-associated apoptosis of CD4+ T cells and CD4ᵈⁱᵐCD8ᵇʳⁱᵍʰᵗ T cells, a population that is infected by HIV. We found that the induction of β-catenin, via a 6-bromoindirubin-3-oxime (BIO), significantly rescued HIV-infected CD4+ and CD4ᵈⁱᵐCD8ᵇʳⁱᵍʰᵗ T cells from apoptosis by >40–50%. Further, a small-molecule inhibitor of the Wnt/β-catenin pathway (PNU-74654) reversed BIO-mediated protection from HIV-associated apoptosis. BIO also induced Bcl-xL, an anti-apoptotic protein, and a target gene of Wnt/β-catenin, in CD4+ and CD4ᵈⁱᵐCD8ᵇʳⁱᵍʰᵗ T cells by approximately 3-fold. Inhibiting Bcl-xL by WEHI-539 abrogated β-catenin-mediated apoptotic protection in infected CD4+ and CD4ᵈⁱᵐCD8ᵇʳⁱᵍʰᵗ T cells. Collectively, these findings demonstrate that engaging Wnt/β-catenin signaling in HIV-infected T cells protects them from HIV-associated apoptosis by inducing Bcl-xL.
    Keywords HIV infections ; apoptosis ; genes ; pro-apoptotic proteins ; transcription (genetics)
    Language English
    Dates of publication 2022-0702
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2516098-9
    ISSN 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v14071469
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: CD4

    Albalawi, Yasmeen A / Narasipura, Srinivas D / Olivares, Leannie J / Al-Harthi, Lena

    Journal of virology

    2022  Volume 96, Issue 15, Page(s) e0080422

    Abstract: ... ...

    Abstract CD4
    MeSH term(s) Animals ; Brain/immunology ; Brain/metabolism ; Brain/virology ; CD4 Antigens ; CD8 Antigens ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; CX3C Chemokine Receptor 1/metabolism ; Cell Movement ; HIV Infections/immunology ; HIV Infections/virology ; HIV-1/pathogenicity ; Humans ; Interleukin Receptor Common gamma Subunit/deficiency ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Proviruses/genetics ; Proviruses/isolation & purification ; Receptors, CXCR3/metabolism ; Receptors, Lymphocyte Homing/metabolism ; Viral Tropism
    Chemical Substances CD4 Antigens ; CD8 Antigens ; CX3C Chemokine Receptor 1 ; Cx3cr1 protein, mouse ; Cxcr3 protein, mouse ; Il2rg protein, mouse ; Interleukin Receptor Common gamma Subunit ; Receptors, CXCR3 ; Receptors, Lymphocyte Homing
    Language English
    Publishing date 2022-07-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/jvi.00804-22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: 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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  4. Article ; Online: β-Catenin Restricts Zika Virus Internalization by Downregulating Axl.

    Jimenez, Oscar A / Narasipura, Srinivas D / Barbian, Hannah J / Albalawi, Yasmeen A / Seaton, Melanie S / Robinson, KaReisha F / Al-Harthi, Lena

    Journal of virology

    2021  Volume 95, Issue 17, Page(s) e0070521

    Abstract: The latest outbreak of Zika virus (ZIKV) in the Americas was associated with significant neurologic complications, including microcephaly of newborns. We evaluated mechanisms that regulate ZIKV entry into human fetal astrocytes (HFAs). Astrocytes are key ...

    Abstract The latest outbreak of Zika virus (ZIKV) in the Americas was associated with significant neurologic complications, including microcephaly of newborns. We evaluated mechanisms that regulate ZIKV entry into human fetal astrocytes (HFAs). Astrocytes are key players in maintaining brain homeostasis. We show that the central mediator of canonical Wnt signaling, β-catenin, regulates Axl, a receptor for ZIKV infection of HFAs, at the transcriptional level. In turn, ZIKV inhibited β-catenin, potentially as a mechanism to overcome its restriction of ZIKV internalization through regulation of Axl. This was evident with three ZIKV strains tested but not with a laboratory-adapted strain which has a large deletion in its envelope gene. Finally, we show that β-catenin-mediated Axl-dependent internalization of ZIKV may be of increased importance for brain cells, as it regulated ZIKV infection of astrocytes and human brain microvascular cells but not kidney epithelial (Vero) cells. Collectively, our studies reveal a role for β-catenin in ZIKV infection and highlight a dynamic interplay between ZIKV and β-catenin to modulate ZIKV entry into susceptible target cells.
    MeSH term(s) Animals ; Astrocytes/metabolism ; Astrocytes/virology ; Brain/metabolism ; Brain/virology ; Chlorocebus aethiops ; Fetus/metabolism ; Fetus/virology ; Humans ; Kidney/metabolism ; Kidney/virology ; Vero Cells ; Virus Internalization ; Virus Replication ; Zika Virus/physiology ; Zika Virus Infection/metabolism ; Zika Virus Infection/prevention & control ; Zika Virus Infection/virology ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances CTNNB1 protein, human ; beta Catenin
    Language English
    Publishing date 2021-08-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00705-21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: 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: CD4 dim CD8 bright T cells are inversely associated with neuro-inflammatory markers among people with HIV.

    Albalawi, Yasmeen A / Shull, Tanner / Virdi, Amber K / Subra, Caroline / Mitchell, Julie / Slike, Bonnie M / Jian, Ningbo / Krebs, Shelly J / Sacdalan, Carlo / Ratnaratorn, Nisakorn / Hsu, Denise C / Phanuphak, Nittaya / Spudich, Serena / Trautmann, Lydie / Al-Harthi, Lena

    AIDS (London, England)

    2023  Volume 38, Issue 1, Page(s) 1–7

    Abstract: Objective: HIV-associated neuroinflammation persists in the brain despite suppressive combination antiretroviral therapy (cART). We evaluated associations between a subset of CD8 + T cells, termed CD4 dim CD8 bright T cells, and soluble markers of ... ...

    Abstract Objective: HIV-associated neuroinflammation persists in the brain despite suppressive combination antiretroviral therapy (cART). We evaluated associations between a subset of CD8 + T cells, termed CD4 dim CD8 bright T cells, and soluble markers of immune activation and/or neuroinflammation in the cerebrospinal fluid (CSF) and plasma of people with HIV (PWH).
    Design: Fifteen cART-naive PWH were enrolled and underwent blood draw, lumbar puncture for CSF collection, and neuropsychological tests at week 0 (pre-cART) and 24 weeks after cART initiation.
    Methods: CSF and peripheral blood T cells were evaluated with flow cytometry and soluble markers of immune activation were measured by multiplex and singleplex assays. Spearman bootstrap correlation coefficients with 10 000 resamples were computed and reported with corresponding 95% confidence intervals (CIs) for each marker of interest and T-cell type.
    Results: The frequency of CSF CD4 dim CD8 bright T cells at week 0 was inversely related with CSF neopterin. In contrast, at week 24, CSF CD4 - CD8 + T cells were positively correlated with CSF s100β, a marker of brain injury. In the blood, at week 0, CD4 dim CD8 bright T cells were inversely correlated with MCP-1, IP-10, IL-8, IL-6, G-CSF, and APRIL and positively correlated with plasma RANTES and MMP1. At week 0, the frequency of blood CD4 - CD8 + were positively correlated with CRP and BAFF.
    Conclusion: CD4 dim CD8 bright T cells are associated with some anti-inflammatory properties, whereas CD4 - CD8 + T cells may contribute to inflammation and injury. Assessing the contrast between these two cell populations in neuroHIV may inform targeted therapeutic intervention to reduce neuroinflammation and associated neurocognitive impairment.
    MeSH term(s) Humans ; CD4-Positive T-Lymphocytes ; CD8-Positive T-Lymphocytes ; Cognition ; HIV Infections/complications ; Neuroinflammatory Diseases/etiology
    Language English
    Publishing date 2023-10-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 639076-6
    ISSN 1473-5571 ; 0269-9370 ; 1350-2840
    ISSN (online) 1473-5571
    ISSN 0269-9370 ; 1350-2840
    DOI 10.1097/QAD.0000000000003743
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2228: 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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  6. Article ; Online: Overriding impaired FPR chemotaxis signaling in diabetic neutrophil stimulates infection control in murine diabetic wound.

    Roy, Ruchi / Zayas, Janet / Singh, Sunil K / Delgado, Kaylee / Wood, Stephen J / Mohamed, Mohamed F / Frausto, Dulce M / Albalawi, Yasmeen A / Price, Thea P / Estupinian, Ricardo / Giurini, Eileena F / Kuzel, Timothy M / Zloza, Andrew / Reiser, Jochen / Shafikhani, Sasha H

    eLife

    2022  Volume 11

    Abstract: Infection is a major co-morbidity that contributes to impaired healing in diabetic wounds. Although impairments in diabetic neutrophils have been blamed for this co-morbidity, what causes these impairments and whether they can be overcome, remain largely ...

    Abstract Infection is a major co-morbidity that contributes to impaired healing in diabetic wounds. Although impairments in diabetic neutrophils have been blamed for this co-morbidity, what causes these impairments and whether they can be overcome, remain largely unclear. Diabetic neutrophils, isolated from diabetic individuals, exhibit chemotaxis impairment but this peculiar functional impairment has been largely ignored because it appears to contradict the clinical findings which blame excessive neutrophil influx as a major impediment to healing in chronic diabetic ulcers. Here, we report that exposure to glucose in diabetic range results in impaired chemotaxis signaling through the formyl peptide receptor (FPR) in neutrophils, culminating in reduced chemotaxis and delayed neutrophil trafficking in the wound of
    MeSH term(s) Animals ; Chemokine CCL3/immunology ; Chemotaxis, Leukocyte/immunology ; Diabetes Complications/microbiology ; Diabetes Mellitus, Experimental/immunology ; Glucose/administration & dosage ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology ; Neutrophils/pathology ; Receptors, Formyl Peptide/genetics ; Receptors, Formyl Peptide/immunology ; Signal Transduction/immunology ; Wound Healing/immunology ; Wound Infection/drug therapy ; Wound Infection/etiology ; Wound Infection/microbiology
    Chemical Substances Chemokine CCL3 ; Receptors, Formyl Peptide ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2022-02-03
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.72071
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: IL-12 p40 monomer is different from other IL-12 family members to selectively inhibit IL-12Rβ1 internalization and suppress EAE.

    Mondal, Susanta / Kundu, Madhuchhanda / Jana, Malabendu / Roy, Avik / Rangasamy, Suresh B / Modi, Khushbu K / Wallace, Jennillee / Albalawi, Yasmeen A / Balabanov, Roumen / Pahan, Kalipada

    Proceedings of the National Academy of Sciences of the United States of America

    2020  Volume 117, Issue 35, Page(s) 21557–21567

    Abstract: Multiple sclerosis (MS) is the most common human demyelinating disease of the central nervous system. The IL-12 family of cytokines has four members, which are IL-12 (p40:p35), IL-23 (p40:p19), the p40 monomer (p40), and the p40 homodimer ( ... ...

    Abstract Multiple sclerosis (MS) is the most common human demyelinating disease of the central nervous system. The IL-12 family of cytokines has four members, which are IL-12 (p40:p35), IL-23 (p40:p19), the p40 monomer (p40), and the p40 homodimer (p40
    MeSH term(s) Adult ; Animals ; Cells, Cultured ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Humans ; Interleukin-12/immunology ; Interleukin-12/metabolism ; Interleukin-12 Subunit p40/immunology ; Interleukin-12 Subunit p40/pharmacology ; Interleukin-23/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/blood ; Multiple Sclerosis/immunology ; Protein Binding ; Receptors, Interleukin-12/antagonists & inhibitors ; Receptors, Interleukin-12/immunology ; Recombinant Proteins/pharmacology ; Signal Transduction ; Th17 Cells/drug effects ; Th17 Cells/immunology
    Chemical Substances Interleukin-12 Subunit p40 ; Interleukin-23 ; Receptors, Interleukin-12 ; Recombinant Proteins ; Interleukin-12 (187348-17-0)
    Language English
    Publishing date 2020-08-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2000653117
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: 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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