LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 3 of total 3

Search options

  1. Article ; Online: Macrophage-derived human resistin promotes perivascular adipose tissue dysfunction in experimental inflammatory arthritis.

    Fedoce, Aline G / Veras, Flávio P / Rosa, Marcos H / Schneider, Ayda H / Paiva, Isadora M / Machado, Mirele R / Freitas-Filho, Edismauro G / Silva, Josiane F / Machado, Caio C / Alves-Filho, José C / Cunha, Fernando Q / N Z Ramalho, Leandra / Louzada-Junior, Paulo / Bonavia, Anthony S / Tostes, Rita C

    Biochemical pharmacology

    2024  Volume 224, Page(s) 116245

    Abstract: Cardiovascular disease (CVD) is the leading cause of death in rheumatoid arthritis (RA). Resistin is an adipokine that induces adipose tissue inflammation and activation of monocytes/macrophages via adenylate cyclase-associated protein-1 (CAP1). Resistin ...

    Abstract Cardiovascular disease (CVD) is the leading cause of death in rheumatoid arthritis (RA). Resistin is an adipokine that induces adipose tissue inflammation and activation of monocytes/macrophages via adenylate cyclase-associated protein-1 (CAP1). Resistin levels are increased in RA and might cause perivascular adipose tissue (PVAT) dysfunction, leading to vascular damage and CVD. This study aimed to investigate the role of resistin in promoting PVAT dysfunction by increasing local macrophage and inflammatory cytokines content in antigen-induced arthritis (AIA). Resistin pharmacological effects were assessed by using C57Bl/6J wild-type (WT) mice, humanized resistin mice expressing human resistin in monocytes-macrophages (hRTN
    Language English
    Publishing date 2024-04-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2024.116245
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 19: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: Efferocytosis of SARS-CoV-2-infected dying cells impairs macrophage anti-inflammatory functions and clearance of apoptotic cells.

    Salina, Ana C G / Dos-Santos, Douglas / Rodrigues, Tamara S / Fortes-Rocha, Marlon / Freitas-Filho, Edismauro G / Alzamora-Terrel, Daniel L / Castro, Icaro M S / Fraga da Silva, Thais F C / de Lima, Mikhael H F / Nascimento, Daniele C / Silva, Camila M / Toller-Kawahisa, Juliana E / Becerra, Amanda / Oliveira, Samuel / Caetité, Diego B / Almeida, Leticia / Ishimoto, Adriene Y / Lima, Thais M / Martins, Ronaldo B /
    Veras, Flavio / do Amaral, Natália B / Giannini, Marcela C / Bonjorno, Letícia P / Lopes, Maria I F / Benatti, Maira N / Batah, Sabrina S / Santana, Rodrigo C / Vilar, Fernando C / Martins, Maria A / Assad, Rodrigo L / de Almeida, Sergio C L / de Oliveira, Fabiola R / Arruda Neto, Eurico / Cunha, Thiago M / Alves-Filho, José C / Bonato, Vania L D / Cunha, Fernando Q / Fabro, Alexandre T / Nakaya, Helder I / Zamboni, Dario S / Louzada-Junior, Paulo / Oliveira, Rene D R / Cunha, Larissa D

    eLife

    2022  Volume 11

    Abstract: COVID-19 is a disease of dysfunctional immune responses, but the mechanisms triggering immunopathogenesis are not established. The functional plasticity of macrophages allows this cell type to promote pathogen elimination and inflammation or suppress ... ...

    Abstract COVID-19 is a disease of dysfunctional immune responses, but the mechanisms triggering immunopathogenesis are not established. The functional plasticity of macrophages allows this cell type to promote pathogen elimination and inflammation or suppress inflammation and promote tissue remodeling and injury repair. During an infection, the clearance of dead and dying cells, a process named efferocytosis, can modulate the interplay between these contrasting functions. Here, we show that engulfment of SARS-CoV-2-infected apoptotic cells exacerbates inflammatory cytokine production, inhibits the expression of efferocytic receptors, and impairs continual efferocytosis by macrophages. We also provide evidence supporting that lung monocytes and macrophages from severe COVID-19 patients have compromised efferocytic capacity. Our findings reveal that dysfunctional efferocytosis of SARS-CoV-2-infected cell corpses suppresses macrophage anti-inflammation and efficient tissue repair programs and provides mechanistic insights for the excessive production of pro-inflammatory cytokines and accumulation of tissue damage associated with COVID-19 immunopathogenesis.
    MeSH term(s) Anti-Inflammatory Agents/pharmacology ; Apoptosis ; COVID-19 ; Humans ; Macrophages/metabolism ; Phagocytosis ; SARS-CoV-2
    Chemical Substances Anti-Inflammatory Agents
    Language English
    Publishing date 2022-06-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.74443
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Efferocytosis of SARS-CoV-2-infected dying cells impairs macrophage anti-inflammatory programming and continual clearance of apoptotic cells

    dos-Santos, Douglas / Salina, Ana C. G. / Rodrigues, Tamara S. / Rocha, Marlon F. / Freitas-Filho, Edismauro G. / Alzamora-Terrel, Daniel L. / de Lima, Mikhael H. F. / Nascimento, Daniele B. C. / Castro, Icaro / Silva, Camila M. / Toller-Kawahisa, Juliana E. / Becerra, Amanda / Oliveira, Samuel / Caetite, Diego B. / Almeida, Leticia / Ishimoto, Adriene Y. / Lima, Thais M. / Martins, Ronaldo B. / Veras, Flavio /
    do Amaral, Natalia B. / Giannini, Marcela C. / Bonjorno, Leticia P. / Lopes, Maria I. F. / Benatti, Maira N. / Batah, Sabrina S. / Santana, Rodrigo C. / Vilar, Fernando C. / Martins, Maria A. / Assad, Rodrigo L. / de Almeida, Sergio C. L. / de Oliveira, Fabiola R. / Arruda Neto, Eurico / Cunha, Thiago M. / Alves-Filho, Jose C / Cunha, Fernando Q. / Fabro, Alexandre T. / Nakaya, Helder I / Zamboni, Dario S. / Louzada-Junior, Paulo / Oliveira, Rene D. R. / Cunha, Larissa D.

    medRxiv

    Abstract: COVID-19 is a disease of dysfunctional immune responses, but the mechanisms triggering immunopathogenesis are not established. The functional plasticity of macrophages allows this cell type to promote pathogen elimination and inflammation or suppress ... ...

    Abstract COVID-19 is a disease of dysfunctional immune responses, but the mechanisms triggering immunopathogenesis are not established. The functional plasticity of macrophages allows this cell type to promote pathogen elimination and inflammation or suppress inflammation and promote tissue remodeling and injury repair. During an infection, the clearance of dead and dying cells, a process named efferocytosis, can modulate the interplay between these contrasting functions. Here, we show that engulfment of SARS-CoV2-infected apoptotic cells (AC) exacerbates inflammatory cytokine production, inhibits the expression of efferocytic receptors, and impairs continual efferocytosis by macrophages. We also provide evidence that monocytes from severe COVID-19 patients express reduced levels of efferocytic receptors and fail to uptake AC. Our findings reveal that dysfunctional efferocytosis of SARS-CoV-2-infected cell corpses suppress macrophage anti-inflammation and efficient tissue repair programs and provide mechanistic insights for the pathogenesis of the hyperinflammation and extensive tissue damage associated with COVID-19.
    Keywords covid19
    Language English
    Publishing date 2021-02-23
    Publisher Cold Spring Harbor Laboratory Press
    Document type Article ; Online
    DOI 10.1101/2021.02.18.21251504
    Database COVID19

    Full text online

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top