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  1. Article: NETosis and the Immune System in COVID-19: Mechanisms and Potential Treatments.

    Gillot, Constant / Favresse, Julien / Mullier, François / Lecompte, Thomas / Dogné, Jean-Michel / Douxfils, Jonathan

    Frontiers in pharmacology

    2021  Volume 12, Page(s) 708302

    Abstract: ... of COVID-19 by promoting a pro-inflammatory and a procoagulant state leading to multiorgan failure ... observed in severe COVID-19 patients. These two elements therefore represent possible targets for treatment ... NETosis is a form of neutrophil death leading to the release of extracellular chromatin and ...

    Abstract NETosis is a form of neutrophil death leading to the release of extracellular chromatin and the assembling of proteins, including antiviral proteins, primed by an initial pathogenic stimulus. Under certain specific conditions, neutrophils can exhibit a double-edged activity. This event has been implicated in COVID-19 among other conditions. Neutrophil extracellular traps (NETs) are involved in the pathogenesis of COVID-19 by promoting a pro-inflammatory and a procoagulant state leading to multiorgan failure. This particular form of host defense promoted by neutrophils is closely related to the well-known cytokine storm observed in severe COVID-19 patients. These two elements therefore represent possible targets for treatment of severe SARS-CoV-2 infections.
    Language English
    Publishing date 2021-08-05
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2021.708302
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: NETosis promotes chronic inflammation and fibrosis in systemic lupus erythematosus and COVID-19.

    Lin, Huiqing / Liu, Jiejie / Li, Ning / Zhang, Birong / Nguyen, Van Dien / Yao, Peipei / Feng, Jiangpeng / Liu, Qianyun / Chen, Yu / Li, Guang / Zhou, You / Zhou, Li

    Clinical immunology (Orlando, Fla.)

    2023  Volume 254, Page(s) 109687

    Abstract: ... biopsies from individuals with SLE, COVID-19-induced pulmonary fibrosis, and idiopathic pulmonary fibrosis ... extracellular trap formation, showing similar enrichment signature between SLE and COVID-19. The abundance ... of Neutrophil extracellular traps (NETs) was much higher in the lungs of individuals with SLE and COVID-19 ...

    Abstract Pulmonary fibrosis, a serious complication of systemic lupus erythematosus (SLE) and coronavirus disease 2019 (COVID-19), leads to irreversible lung damage. However, the underlying mechanism of this condition remains unclear. In this study, we revealed the landscape of transcriptional changes in lung biopsies from individuals with SLE, COVID-19-induced pulmonary fibrosis, and idiopathic pulmonary fibrosis (IPF) using histopathology and RNA sequencing, respectively. Despite the diverse etiologies of these diseases, lung expression of matrix metalloproteinase genes in these diseases showed similar patterns. Particularly, the differentially expressed genes were significantly enriched in the pathway of neutrophil extracellular trap formation, showing similar enrichment signature between SLE and COVID-19. The abundance of Neutrophil extracellular traps (NETs) was much higher in the lungs of individuals with SLE and COVID-19 compared to those with IPF. In-depth transcriptome analyses revealed that NETs formation pathway promotes epithelial-mesenchymal transition (EMT). Furthermore, stimulation with NETs significantly up-regulated α-SMA, Twist, Snail protein expression, while decreasing the expression of E-cadherin protein in vitro. This indicates that NETosis promotes EMT in lung epithelial cells. Given drugs that are efficacious in degrading damaged NETs or inhibiting NETs production, we identified a few drug targets that were aberrantly expressed in both SLE and COVID-19. Among these targets, the JAK2 inhibitor Tofacitinib could effectively disrupted the process of NETs and reversed NET-induced EMT in lung epithelial cells. These findings support that the NETs/EMT axis, activated by SLE and COVID-19, contributes to the progression of pulmonary fibrosis. Our study also highlights that JAK2 as a potential target for the treatment of fibrosis in these diseases.
    MeSH term(s) Humans ; Neutrophils/metabolism ; Pulmonary Fibrosis/etiology ; Pulmonary Fibrosis/metabolism ; COVID-19/pathology ; Lupus Erythematosus, Systemic/metabolism ; Inflammation/metabolism ; Fibrosis
    Language English
    Publishing date 2023-07-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2023.109687
    Database MEDical Literature Analysis and Retrieval System OnLINE

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