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  1. Article: RSV infection does not induce EMT.

    Talukdar, Sattya N / McGregor, Brett / Osan, Jaspreet K / Hur, Junguk / Mehedi, Masfique

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Respiratory syncytial virus (RSV) infection does not cause severe disease in most of us despite suffering from multiple RSV infections in our lives. However, infants, young children, older adults, and immunocompromised patients are unfortunately ... ...

    Abstract Respiratory syncytial virus (RSV) infection does not cause severe disease in most of us despite suffering from multiple RSV infections in our lives. However, infants, young children, older adults, and immunocompromised patients are unfortunately vulnerable to RSV-associated severe diseases. A recent study suggested that RSV infection causes cell expansion, resulting in bronchial wall thickening
    Language English
    Publishing date 2023-03-14
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.03.13.532506
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Respiratory Syncytial Virus Infection Does Not Induce Epithelial-Mesenchymal Transition.

    Talukdar, Sattya N / McGregor, Brett / Osan, Jaspreet K / Hur, Junguk / Mehedi, Masfique

    Journal of virology

    2023  Volume 97, Issue 7, Page(s) e0039423

    Abstract: Respiratory syncytial virus (RSV) infection does not cause severe disease in most of us despite suffering from multiple RSV infections during our lives. However, infants, young children, older adults, and immunocompromised patients are unfortunately ... ...

    Abstract Respiratory syncytial virus (RSV) infection does not cause severe disease in most of us despite suffering from multiple RSV infections during our lives. However, infants, young children, older adults, and immunocompromised patients are unfortunately vulnerable to RSV-associated severe diseases. A recent study suggested that RSV infection causes cell expansion, resulting in bronchial wall thickening
    MeSH term(s) Aged ; Child ; Child, Preschool ; Humans ; Infant ; Actins/metabolism ; Cell Line ; Epithelial Cells/metabolism ; Epithelial-Mesenchymal Transition ; Respiratory Syncytial Virus Infections/metabolism ; Respiratory Syncytial Viruses/metabolism ; Transforming Growth Factor beta1
    Chemical Substances Actins ; Transforming Growth Factor beta1
    Language English
    Publishing date 2023-06-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/jvi.00394-23
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Immunohistochemistry for protein detection in PFA-fixed paraffin-embedded SARS-CoV-2-infected COPD airway epithelium.

    Osan, Jaspreet Kaur / DeMontigny, Beth Ann / Mehedi, Masfique

    STAR protocols

    2021  Volume 2, Issue 3, Page(s) 100663

    Abstract: Patients with chronic lung disease are vulnerable to getting severe diseases associated with SARS-CoV-2 infection. Here, we describe protocols for subculturing and differentiating primary normal human bronchial epithelial (NHBE) cells of patients with ... ...

    Abstract Patients with chronic lung disease are vulnerable to getting severe diseases associated with SARS-CoV-2 infection. Here, we describe protocols for subculturing and differentiating primary normal human bronchial epithelial (NHBE) cells of patients with chronic obstructive lung disease. The differentiation of NHBE cells in air-liquid interface mimics an
    MeSH term(s) Bronchi/metabolism ; Bronchi/pathology ; Bronchi/virology ; COVID-19/complications ; COVID-19/metabolism ; COVID-19/virology ; Coronavirus Nucleocapsid Proteins/analysis ; Coronavirus Nucleocapsid Proteins/metabolism ; Epithelium/metabolism ; Epithelium/pathology ; Epithelium/virology ; Humans ; Immunohistochemistry ; Paraffin Embedding ; Phosphoproteins/analysis ; Phosphoproteins/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/pathology ; Pulmonary Disease, Chronic Obstructive/virology ; SARS-CoV-2/isolation & purification ; Virus Replication
    Chemical Substances Coronavirus Nucleocapsid Proteins ; Phosphoproteins ; nucleocapsid phosphoprotein, SARS-CoV-2
    Language English
    Publishing date 2021-06-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2021.100663
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Immunohistochemistry for protein detection in PFA-fixed paraffin-embedded SARS-CoV-2-infected COPD airway epithelium

    Jaspreet Kaur Osan / Beth Ann DeMontigny / Masfique Mehedi

    STAR Protocols, Vol 2, Iss 3, Pp 100663- (2021)

    2021  

    Abstract: Summary: Patients with chronic lung disease are vulnerable to getting severe diseases associated with SARS-CoV-2 infection. Here, we describe protocols for subculturing and differentiating primary normal human bronchial epithelial (NHBE) cells of ... ...

    Abstract Summary: Patients with chronic lung disease are vulnerable to getting severe diseases associated with SARS-CoV-2 infection. Here, we describe protocols for subculturing and differentiating primary normal human bronchial epithelial (NHBE) cells of patients with chronic obstructive lung disease. The differentiation of NHBE cells in air-liquid interface mimics an in vivo airway and provides an in vitro model for studying SARS-CoV-2 infection. We also describe a protocol for detecting proteins in the sectioned epithelium for detailing SARS-CoV-2 infection-induced pathobiology with a vertical view.
    Keywords Health Sciences ; Immunology ; Microbiology ; Microscopy ; Antibody ; Science (General) ; Q1-390
    Language English
    Publishing date 2021-09-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Role of ARP2/3 Complex-Driven Actin Polymerization in RSV Infection

    Autumn Paluck / Jaspreet Osan / Lauren Hollingsworth / Sattya Narayan Talukdar / Ali Al Saegh / Masfique Mehedi

    Pathogens, Vol 11, Iss 26, p

    2022  Volume 26

    Abstract: Respiratory syncytial virus (RSV) is the leading viral agent causing bronchiolitis and pneumonia in children under five years old worldwide. The RSV infection cycle starts with macropinocytosis-based entry into the host airway epithelial cell membrane, ... ...

    Abstract Respiratory syncytial virus (RSV) is the leading viral agent causing bronchiolitis and pneumonia in children under five years old worldwide. The RSV infection cycle starts with macropinocytosis-based entry into the host airway epithelial cell membrane, followed by virus transcription, replication, assembly, budding, and spread. It is not surprising that the host actin cytoskeleton contributes to different stages of the RSV replication cycle. RSV modulates actin-related protein 2/3 (ARP2/3) complex-driven actin polymerization for a robust filopodia induction on the infected lung epithelial A549 cells, which contributes to the virus’s budding, and cell-to-cell spread. Thus, a comprehensive understanding of RSV-induced cytoskeletal modulation and its role in lung pathobiology may identify novel intervention strategies. This review will focus on the role of the ARP2/3 complex in RSV’s pathogenesis and possible therapeutic targets to the ARP2/3 complex for RSV.
    Keywords cytoskeleton dynamics ; filopodia ; ARP2/3 complex ; actin polymerization ; cell-to-cell spread ; RSV ; Medicine ; R
    Subject code 570
    Language English
    Publishing date 2022-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Role of ARP2/3 Complex-Driven Actin Polymerization in RSV Infection.

    Paluck, Autumn / Osan, Jaspreet / Hollingsworth, Lauren / Talukdar, Sattya Narayan / Saegh, Ali Al / Mehedi, Masfique

    Pathogens (Basel, Switzerland)

    2021  Volume 11, Issue 1

    Abstract: Respiratory syncytial virus (RSV) is the leading viral agent causing bronchiolitis and pneumonia in children under five years old worldwide. The RSV infection cycle starts with macropinocytosis-based entry into the host airway epithelial cell membrane, ... ...

    Abstract Respiratory syncytial virus (RSV) is the leading viral agent causing bronchiolitis and pneumonia in children under five years old worldwide. The RSV infection cycle starts with macropinocytosis-based entry into the host airway epithelial cell membrane, followed by virus transcription, replication, assembly, budding, and spread. It is not surprising that the host actin cytoskeleton contributes to different stages of the RSV replication cycle. RSV modulates actin-related protein 2/3 (ARP2/3) complex-driven actin polymerization for a robust filopodia induction on the infected lung epithelial A549 cells, which contributes to the virus's budding, and cell-to-cell spread. Thus, a comprehensive understanding of RSV-induced cytoskeletal modulation and its role in lung pathobiology may identify novel intervention strategies. This review will focus on the role of the ARP2/3 complex in RSV's pathogenesis and possible therapeutic targets to the ARP2/3 complex for RSV.
    Language English
    Publishing date 2021-12-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens11010026
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  7. Article ; Online: Goblet Cell Hyperplasia Increases SARS-CoV-2 Infection in Chronic Obstructive Pulmonary Disease.

    Osan, Jaspreet / Talukdar, Sattya N / Feldmann, Friederike / DeMontigny, Beth Ann / Jerome, Kailey / Bailey, Kristina L / Feldmann, Heinz / Mehedi, Masfique

    Microbiology spectrum

    2022  Volume 10, Issue 4, Page(s) e0045922

    Abstract: Chronic obstructive pulmonary disease (COPD) is one of the underlying conditions in adults of any age that place them at risk for developing severe illnesses associated with COVID-19. To determine whether SARS-CoV-2's cellular tropism plays a critical ... ...

    Abstract Chronic obstructive pulmonary disease (COPD) is one of the underlying conditions in adults of any age that place them at risk for developing severe illnesses associated with COVID-19. To determine whether SARS-CoV-2's cellular tropism plays a critical role in severe pathophysiology in the lung, we investigated its host cell entry receptor distribution in the bronchial airway epithelium of healthy adults and high-risk adults (those with COPD). We found that SARS-CoV-2 preferentially infects goblet cells in the bronchial airway epithelium, as mostly goblet cells harbor the entry receptor angiotensin-converting enzyme 2 (ACE2) and its cofactor transmembrane serine protease 2 (TMPRSS2). We also found that SARS-CoV-2 replication was substantially increased in the COPD bronchial airway epithelium, likely due to COPD-associated goblet cell hyperplasia. Likewise, SARS-CoV and Middle East respiratory syndrome (MERS-CoV) infection increased disease pathophysiology (e.g., syncytium formation) in the COPD bronchial airway epithelium. Our results reveal that goblet cells play a critical role in SARS-CoV-2-induced pathophysiology in the lung.
    MeSH term(s) Adult ; COVID-19 ; Goblet Cells/metabolism ; Humans ; Hyperplasia/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism ; SARS-CoV-2
    Language English
    Publishing date 2022-07-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2807133-5
    ISSN 2165-0497 ; 2165-0497
    ISSN (online) 2165-0497
    ISSN 2165-0497
    DOI 10.1128/spectrum.00459-22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: RSV-induced expanded ciliated cells contribute to bronchial wall thickening.

    Talukdar, Sattya N / Osan, Jaspreet / Ryan, Ken / Grove, Bryon / Perley, Danielle / Kumar, Bony D / Yang, Shirley / Dallman, Sydney / Hollingsworth, Lauren / Bailey, Kristina L / Mehedi, Masfique

    Virus research

    2023  Volume 327, Page(s) 199060

    Abstract: Viral infection, particularly respiratory syncytial virus (RSV), causes inflammation in the bronchiolar airways (bronchial wall thickening, also known as bronchiolitis). This bronchial wall thickening is a common pathophysiological feature in RSV ... ...

    Abstract Viral infection, particularly respiratory syncytial virus (RSV), causes inflammation in the bronchiolar airways (bronchial wall thickening, also known as bronchiolitis). This bronchial wall thickening is a common pathophysiological feature in RSV infection, but it causes more fatalities in infants than in children and adults. However, the molecular mechanism of RSV-induced bronchial wall thickening remains unknown, particularly in healthy adults. Using highly differentiated pseudostratified airway epithelium generated from primary human bronchial epithelial cells, we revealed RSV-infects primarily ciliated cells. The infected ciliated cells expanded substantially without compromising epithelial membrane integrity and ciliary functions and contributed to the increased height of the airway epithelium. Furthermore, we identified multiple factors, e.g., cytoskeletal (ARP2/3-complex-driven actin polymerization), immunological (IP10/CXCL10), and viral (NS2), contributing to RSV-induced uneven epithelium height increase in vitro. Thus, RSV-infected expanded cells contribute to a noncanonical inflammatory phenotype, which contributes to bronchial wall thickening in the airway, and is termed cytoskeletal inflammation.
    MeSH term(s) Child ; Infant ; Adult ; Humans ; Respiratory Syncytial Virus, Human/physiology ; Respiratory Syncytial Virus Infections ; Epithelial Cells ; Epithelium ; Inflammation
    Language English
    Publishing date 2023-02-14
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 605780-9
    ISSN 1872-7492 ; 0168-1702
    ISSN (online) 1872-7492
    ISSN 0168-1702
    DOI 10.1016/j.virusres.2023.199060
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1965: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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  9. Article ; Online: RSV-induced Expanded Ciliated Cells Contribute to Bronchial Wall Thickening

    Talukdar, Sattya N. / Osan, Jaspreet / Ryan, Ken / Grove, Bryon / Perley, Danielle / Kumar, Bony D. / Yang, Shirley / Dallman, Sydney / Hollingsworth, Lauren / Bailey, Kristina L. / Mehedi, Masfique

    Virus Research. 2023, p.199060-

    2023  , Page(s) 199060–

    Abstract: Viral infection, particularly respiratory syncytial virus (RSV), causes inflammation in the bronchiolar airways (bronchial wall thickening, also known as bronchiolitis). This bronchial wall thickening is a common pathophysiological feature in RSV ... ...

    Abstract Viral infection, particularly respiratory syncytial virus (RSV), causes inflammation in the bronchiolar airways (bronchial wall thickening, also known as bronchiolitis). This bronchial wall thickening is a common pathophysiological feature in RSV infection, but it causes more fatalities in infants than in children and adults. However, the molecular mechanism of RSV-induced bronchial wall thickening remains unknown, particularly in healthy adults. Using highly differentiated pseudostratified airway epithelium generated from primary human bronchial epithelial cells, we revealed RSV-infects primarily ciliated cells. The infected ciliated cells expanded substantially without compromising epithelial membrane integrity and ciliary functions and contributed to the increased height of the airway epithelium. Furthermore, we identified multiple factors, e.g., cytoskeletal (ARP2/3-complex-driven actin polymerization), immunological (IP10/CXCL10), and viral (NS2), contributing to RSV-induced uneven epithelium height increase in vitro. Thus, RSV-infected expanded cells contribute to a noncanonical inflammatory phenotype, which contributes to bronchial wall thickening in the airway, and is termed cytoskeletal inflammation.
    Keywords Respiratory syncytial virus ; actin ; bronchiolitis ; cytoskeleton ; epithelium ; humans ; inflammation ; phenotype ; polymerization ; research ; viruses
    Language English
    Publishing place Elsevier B.V.
    Document type Article ; Online
    Note Pre-press version ; Use and reproduction
    ZDB-ID 605780-9
    ISSN 1872-7492 ; 0168-1702
    ISSN (online) 1872-7492
    ISSN 0168-1702
    DOI 10.1016/j.virusres.2023.199060
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1965: Show issues Location:
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  10. Article: Role of ARP2/3 Complex-Driven Actin Polymerization in RSV Infection

    Paluck, Autumn / Osan, Jaspreet / Hollingsworth, Lauren / Talukdar, Sattya Narayan / Saegh, Ali Al / Mehedi, Masfique

    Pathogens. 2021 Dec. 26, v. 11, no. 1

    2021  

    Abstract: Respiratory syncytial virus (RSV) is the leading viral agent causing bronchiolitis and pneumonia in children under five years old worldwide. The RSV infection cycle starts with macropinocytosis-based entry into the host airway epithelial cell membrane, ... ...

    Abstract Respiratory syncytial virus (RSV) is the leading viral agent causing bronchiolitis and pneumonia in children under five years old worldwide. The RSV infection cycle starts with macropinocytosis-based entry into the host airway epithelial cell membrane, followed by virus transcription, replication, assembly, budding, and spread. It is not surprising that the host actin cytoskeleton contributes to different stages of the RSV replication cycle. RSV modulates actin-related protein 2/3 (ARP2/3) complex-driven actin polymerization for a robust filopodia induction on the infected lung epithelial A549 cells, which contributes to the virus’s budding, and cell-to-cell spread. Thus, a comprehensive understanding of RSV-induced cytoskeletal modulation and its role in lung pathobiology may identify novel intervention strategies. This review will focus on the role of the ARP2/3 complex in RSV’s pathogenesis and possible therapeutic targets to the ARP2/3 complex for RSV.
    Keywords Respiratory syncytial virus ; actin ; bronchiolitis ; cell membranes ; epithelial cells ; epithelium ; lungs ; microfilaments ; pathogenesis ; pneumonia ; polymerization ; pseudopodia ; therapeutics ; viruses
    Language English
    Dates of publication 2021-1226
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens11010026
    Database NAL-Catalogue (AGRICOLA)

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