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Chloroquine Inhibits the Release of Inflammatory Cytokines by Human Lung Explants
Grassin-Delyle et al., Clinical Infectious Diseases, doi:10.1093/cid/ciaa546 (Ex Vivo)
Grassin-Delyle et al., Chloroquine Inhibits the Release of Inflammatory Cytokines by Human Lung Explants, Clinical Infectious Diseases, doi:10.1093/cid/ciaa546 (Ex Vivo)
May 2020   Source   PDF  
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On human lung parenchymal explants, CQ concentration clinically achievable in the lung (100µM) inhibited the lipopolysaccharide-induced release of TNF-ɑ (by 76%), IL-6 (by 68%), CCL2 (by 72%), and CCL3 (by 67%). In addition to antiviral activity, CQ may also mitigate the cytokine storm associated with severe pneumonia caused by coronaviruses.
Grassin-Delyle et al., 8 May 2020, peer-reviewed, 8 authors.
Ex Vivo studies are an important part of preclinical research, however results may be very different in vivo.
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Abstract: Chloroquine inhibits the release of inflammatory cytokines cr ip Marion Brollo3, Emilie Catherinot1, Edouard Sage1,4, Louis-Jean Couderc1,3, an us Emmanuel Naline1,3, Philippe Devillier1,3 Department of Respiratory Diseases, Foch Hospital, Suresnes, France. 2 INSERM Infection & inflammation, Département de Biotechnologie de la Santé, University Paris- M 1 Saclay, Montigny-le-Bretonneux, France. Laboratory of Research in Respiratory Pharmacology, Exhalomics Facility, Foch Hospital, University ed 3 Paris-Saclay, Suresnes, France. UMR0892, INRAE, University Paris-Saclay, Jouy-en-Josas, France. ce pt 4 Ac Address correspondence to: Professor Philippe Devillier, Laboratory of Research in Respiratory Pharmacology, Foch Hospital, University Paris-Saclay, 11 rue Guillaume Lenoir, F-92150 Suresnes, France. Tel: (+33)146252791, Fax: (+33)140999657. E-mail: © The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: Stanislas Grassin-Delyle1,2, Hélène Salvator1,3, t by human lung explants Abstract On human lung parenchymal explants, chloroquine concentration clinically achievable in the lung (by 72%) and CCL3 (by 67%). Beside its antiviral activity, chloroquine might also mitigate the cytokine cr ip t storm associated with severe pneumonia caused by coronaviruses. Keywords: chloroquine; lung explant; tumour necrosis factor-alpha; interleukin-6; Ac ce pt ed M an us chemokine; lipopolysaccharide. 2 (100 M) inhibited the lipopolysaccharide-induced release of TNF-by 76%), IL-6 (by 68%), CCL2 The severe pneumonia caused by severe acute respiratory syndrome coronaviruses (SARSCOVs) features rapid viral replication and then an intense, prolonged cytokine/chemokine response cytokines, such as interleukin (IL)-6, tumour necrosis factor-alpha (TNF-α), macrophage inflammatory protein-1α (CCL3), and monocyte chemoattractant protein 1 (CCL2) [1-4]. Reports that cr ip t plasma cytokine levels are higher in patients requiring intensive care than those not requiring intensive care, suggest that the cytokine storm is linked to disease severity [3]. Hence, dysregulated and/or exaggerated cytokine and chemokine responses to SARS-CoV infection might have a major us influence on the pathogenesis of coronavirus disease and the associated morbidity and mortality [1- an 4]. The antimalarial drugs chloroquine and hydroxychloroquine have been used to treat patients M infected with SARS-CoV-2. Given the efficacy observed in trials conducted in China, chloroquine is to be included in the forthcoming version of the Chinese national guidelines for the prevention, ed diagnosis, and treatment of pneumonia caused by SARS-CoV-2 [5]. Chloroquine will probably be the first compound to be widely used in China and worldwide as the first-line treatment of severe SARS- ce pt CoV-2 infections due to its broad availability, low cost, and low frequency of adverse drug reactions [6]. The Food and Drug Administration also encourages the use of chloroquine and hydroxychloroquine..
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