作者
Bruna M Silva, Giovanni F Gomes, Flavio P Veras, Seppe Cambier, Gabriel VL Silva, Andreza U Quadros, Diego B Caetité, Daniele C Nascimento, Camilla M Silva, Juliana C Silva, Samara Damasceno, Ayda H Schneider, Fabio Beretta, Sabrina S Batah, Icaro MS Castro, Isadora M Paiva, Tamara Rodrigues, Ana Salina, Ronaldo Martins, Guilherme CM Cebinelli, Naira L Bibo, Daniel M Jorge, Helder I Nakaya, Dario S Zamboni, Luiz O Leiria, Alexandre T Fabro, José C Alves-Filho, Eurico Arruda, Paulo Louzada-Junior, Renê D Oliveira, Larissa D Cunha, Pierre Van Mol, Lore Vanderbeke, Simon Feys, Els Wauters, Laura Brandolini, Andrea Aramini, Fernando Q Cunha, Jörg Köhl, Marcello Allegretti, Diether Lambrechts, Joost Wauters, Paul Proost, Thiago M Cunha
发表日期
2023/6/15
期刊
The Journal of Clinical Investigation
卷号
133
期号
12
出版商
American Society for Clinical Investigation
简介
Patients with severe COVID-19 develop acute respiratory distress syndrome (ARDS) that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that complement component 5a (C5a), through its cellular receptor C5aR1, has potent proinflammatory actions and plays immunopathological roles in inflammatory diseases, we investigated whether the C5a/C5aR1 pathway could be involved in COVID-19 pathophysiology. C5a/C5aR1 signaling increased locally in the lung, especially in neutrophils of critically ill patients with COVID-19 compared with patients with influenza infection, as well as in the lung tissue of K18-hACE2 Tg mice (Tg mice) infected with SARS-CoV-2. Genetic and pharmacological inhibition of C5aR1 signaling ameliorated lung immunopathology in Tg-infected mice. Mechanistically, we found that C5aR1 signaling drives neutrophil extracellular traps-dependent (NETs …
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BM Silva, GF Gomes, FP Veras, S Cambier, GVL Silva… - The Journal of Clinical Investigation, 2023