Association of COVID-19 inflammation with activation of the C5a-C5aR1 axis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-07-29

AUTHORS

Julien Carvelli, Olivier Demaria, Frédéric Vély, Luciana Batista, Nassima Chouaki Benmansour, Joanna Fares, Sabrina Carpentier, Marie-Laure Thibult, Ariane Morel, Romain Remark, Pascale André, Agnès Represa, Christelle Piperoglou, Laura Assante Miranda, William Baron, Nourhène Belaid, Clarisse Caillet, Flavien Caraguel, Barbara Carrette, Florent Carrette, Fabien Chanuc, Rachel Courtois, Aurore Fenis, Marilyn Giordano, Mathilde Girard-Madoux, Marc Giraudon-Paoli, Nicolas Gourdin, Gwendoline Grondin, Franceline Guillot, Guillaume Habif, Solène Jaubert, Julie Lopez, Mélanie Le Van, Naouel Lovera, Marine Mansuy, Elodie Bonnet, Audrey Sansaloni, Annick Reboul, Emmanuel Mitry, Camille Nekkar-Constant, Valentine Péri, Paul Ricaut, Léa Simon, Jean-Baptiste Vallier, Marie Vétizou, Robert Zerbib, Sophie Ugolini, Marion Etiennot, Justine Galluso, Luc Lyonnet, Jean-Marie Forel, Laurent Papazian, Lionel Velly, Baptiste André, Antoine Briantais, Benoit Faucher, Estelle Jean, Julie Seguier, Veronique Veit, Jean-Robert Harlé, Boris Pastorino, Clémence Delteil, Laurent Daniel, Jean-Paul Boudsocq, Axelle Clerc, Emmanuel Delmond, Pierre-Olivier Vidal, Hélène Savini, Bruno Coutard, Pierre Yves Cordier, Erwan Le Dault, Christophe Guervilly, Pierre Simeone, Marc Gainnier, Yannis Morel, Mikael Ebbo, Nicolas Schleinitz, Eric Vivier

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in a pandemic1. The C5a complement factor and its receptor C5aR1 (also known as CD88) have a key role in the initiation and maintenance of several inflammatory responses by recruiting and activating neutrophils and monocytes1. Here we provide a longitudinal analysis of immune responses, including phenotypic analyses of immune cells and assessments of the soluble factors that are present in the blood and bronchoalveolar lavage fluid of patients at various stages of COVID-19 severity, including those who were paucisymptomatic or had pneumonia or acute respiratory distress syndrome. The levels of soluble C5a were increased in proportion to the severity of COVID-19 and high expression levels of C5aR1 receptors were found in blood and pulmonary myeloid cells, which supports a role for the C5a-C5aR1 axis in the pathophysiology of acute respiratory distress syndrome. Anti-C5aR1 therapeutic monoclonal antibodies prevented the C5a-mediated recruitment and activation of human myeloid cells, and inhibited acute lung injury in human C5aR1 knock-in mice. These results suggest that blockade of the C5a-C5aR1 axis could be used to limit the infiltration of myeloid cells in damaged organs and prevent the excessive lung inflammation and endothelialitis that are associated with acute respiratory distress syndrome in patients with COVID-19. More... »

PAGES

146-150

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41586-020-2600-6

    DOI

    http://dx.doi.org/10.1038/s41586-020-2600-6

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1129716741

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/32726800


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    38 schema:description Coronavirus disease 2019 (COVID-19) is a disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in a pandemic<sup>1</sup>. The C5a complement factor and its receptor C5aR1 (also known as CD88) have a key role in the initiation and maintenance of several inflammatory responses by recruiting and activating neutrophils and monocytes<sup>1</sup>. Here we provide a longitudinal analysis of immune responses, including phenotypic analyses of immune cells and assessments of the soluble factors that are present in the blood and bronchoalveolar lavage fluid of patients at various stages of COVID-19 severity, including those who were paucisymptomatic or had pneumonia or acute respiratory distress syndrome. The levels of soluble C5a were increased in proportion to the severity of COVID-19 and high expression levels of C5aR1 receptors were found in blood and pulmonary myeloid cells, which supports a role for the C5a-C5aR1 axis in the pathophysiology of acute respiratory distress syndrome. Anti-C5aR1 therapeutic monoclonal antibodies prevented the C5a-mediated recruitment and activation of human myeloid cells, and inhibited acute lung injury in human C5aR1 knock-in mice. These results suggest that blockade of the C5a-C5aR1 axis could be used to limit the infiltration of myeloid cells in damaged organs and prevent the excessive lung inflammation and endothelialitis that are associated with acute respiratory distress syndrome in patients with COVID-19.
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    46 C5a
    47 C5a complement factor
    48 C5a-C5aR1
    49 C5a-C5aR1 axis
    50 C5aR1
    51 C5aR1 receptors
    52 COVID-19
    53 COVID-19 inflammation
    54 COVID-19 severity
    55 activation
    56 acute lung injury
    57 acute respiratory distress syndrome
    58 acute respiratory syndrome coronavirus 2
    59 analysis
    60 antibodies
    61 assessment
    62 association
    63 axis
    64 blockade
    65 blood
    66 bronchoalveolar lavage fluid
    67 cells
    68 complement factors
    69 coronavirus 2
    70 coronavirus disease 2019
    71 disease
    72 disease 2019
    73 distress syndrome
    74 endothelialitis
    75 excessive lung inflammation
    76 expression levels
    77 factors
    78 fluid
    79 high expression levels
    80 human C5aR1
    81 human myeloid cells
    82 immune cells
    83 immune response
    84 infection
    85 infiltration
    86 inflammation
    87 inflammatory response
    88 initiation
    89 injury
    90 key role
    91 lavage fluid
    92 levels
    93 longitudinal analysis
    94 lung inflammation
    95 lung injury
    96 maintenance
    97 mice
    98 monoclonal antibodies
    99 monocytes
    100 myeloid cells
    101 neutrophils
    102 organs
    103 pandemic
    104 pathophysiology
    105 patients
    106 phenotypic analysis
    107 pneumonia
    108 proportion
    109 pulmonary myeloid cells
    110 receptor C5aR1
    111 receptors
    112 recruitment
    113 respiratory distress syndrome
    114 respiratory syndrome coronavirus 2
    115 response
    116 results
    117 role
    118 severe acute respiratory syndrome coronavirus 2
    119 severity
    120 soluble C5a
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