Corpus overview


MeSH Disease

Human Phenotype

There are no HP terms in the subcorpus


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    Adult TRANS post COVID-19 multisystem inflammatory syndrome MESHD and thrombotic microangiopathy MESHD

    Authors: Idris Boudhabhay; Marion Rabant; Louis-Marie Coupry; Armance Marchal; Lubka T Roumenina; Khalil El-Karoui; Mehran Monchi; Franck Pourcine

    doi:10.21203/ Date: 2020-09-11 Source: ResearchSquare

    Background: The coronavirus disease MESHD 2019 pandemic has affected millions of people worldwide but medium and long-term consequences are unknown. Clinical series of Kawasaki-like multisystem inflammatory syndrome MESHD in children TRANS (MIS-C), occurring after SARS-Cov-2 spreading, have been recently described. Case presentation: We describe a case of post COVID-19 MIS in a 46-year-old man, with biopsy-proven renal thrombotic microangiopathy MESHD ( TMA MESHD). Specific complement inhibition with Eculizumab was initiated promptly and lead to a dramatic improvement of renal function. Conclusion: Our case suggests that post COVID-19 MIS is not restricted to children TRANS and that TMA MESHD could play a central role in the pathophysiology of this syndrome

    Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis MESHD

    Authors: Panagiotis Skendros; Alexandros Mitsios; Akrivi Chrysanthopoulou; Dimitrios C Mastellos; Simeon Metallidis; Petros Rafailidis; Maria Ntinopoulou; Eleni Sertaridou; Victoria Tsironidou; Christina Tsigalou; Maria Tektonidou; Theocharis Konstantinidis; Charalampos Papagoras; Ioannis Mitroulis; Georgios Germanidis; John D Lambris; Konstantinos Ritis

    doi:10.1101/2020.06.15.20131029 Date: 2020-06-16 Source: medRxiv

    Emerging data indicate that complement and neutrophils are involved in the maladaptive host immune response that fuels hyper-inflammation MESHD and thrombotic microangiopathy MESHD increasing the mortality rate in coronavirus disease MESHD 2019 (COVID-19). Here, we investigated the interaction between complement and the platelet/neutrophil extracellular traps (NETs)/thrombin axis, using COVID-19 clinical samples, cell-based inhibition studies and NETs/human aortic endothelial cell (HAEC) co-cultures. Increased plasma SERO levels of NETs, TF activity and sC5b-9 were detected in patients. Neutrophils yielded high tissue factor (TF) expression and released NETs carrying functionally active TF. Confirming our ex vivo findings, treatment of control neutrophils with COVID-19 platelet-rich plasma SERO generated TF-bearing NETs that induced thrombotic MESHD activity of HAEC. Thrombin or NETosis inhibition or C5aR1 blockade attenuated platelet-mediated NET-driven thrombogenicity. Serum SERO isolated from COVID-19 patients induces complement activation in vitro, which is consistent with high complement activity in clinical samples. Complement inhibition at the level of C3 with compstatin Cp40 disrupted TF expression in neutrophils. In conclusion, we provide a mechanistic basis that reveals the pivotal role of complement and NETs in COVID-19 immmunothrombosis. This study supports emerging strategies against SARS-CoV-2 infection MESHD that exploit complement therapeutics or NETosis inhibition.

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MeSH Disease
Human Phenotype

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