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  • Response to: ‘Exaggerated neutrophil extracellular trap formation in Kawasaki disease: a key phenomenon behind the outbreak in western countries?’ by Yamashita et al

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Correspondence response
Response to: ‘Exaggerated neutrophil extracellular trap formation in Kawasaki disease: a key phenomenon behind the outbreak in western countries?’ by Yamashita et al
  1. Marie Pouletty1,2,
  2. Glory Dingulu1,
  3. Naim Ouldali1,2,3,
  4. Olivier Corseri1,
  5. Camille Ducrocq1,2,
  6. Ulrich Meinzer1,2,4,5,
  7. Albert Faye1,2,3,
  8. Caroline Galeotti6,
  9. Isabelle Melki1,7,8
  10. Great Paris Region (GPR) Kawa-COVID-19 consortium
    1. 1 General Paediatrics, Department of Infectious Disease and Internal Medicine, Reference centre for Rheumatic, AutoImmune and Systemic diseases in children (RAISE), Robert Debré University Hospital, AP-HP, Paris, France
    2. 2 Université de Paris, UFR de Médecine Paris Nord, 75010 Paris, France
    3. 3 INSERM UMR 1123, ECEVE, Paris, France
    4. 4 Center for Research on Inflammation, UMR1149, INSERM, Paris, France
    5. 5 Biology and Genetics of Bacterial Cell Wall Unit, Pasteur Institute, Paris, France
    6. 6 Department of Pediatric Rheumatology, Reference centre for Autoinflammatory diseases and amyloidosis (CEREMAIA), Hôpital Bicêtre, AP-HP, Le Kremlin-Bicêtre, France
    7. 7 Paediatric Hematology-Immunology and Rheumatology Department, Reference centre for Rheumatic, AutoImmune and Systemic diseases in children (RAISE), Paris, France, Necker-Enfants-Malades University Hospital, AP-HP, Paris, France
    8. 8 Laboratory of Neurogenetics and Neuroinflammation, Imagine Institute, Paris, France
    1. Correspondence to Isabelle Melki, General Paediatrics, Infectious Diseases and Internal Medicine, Hopital Universitaire Robert Debre, Paris, F-75019, France; isabelle.melki{at}aphp.fr

    https://doi.org/10.1136/annrheumdis-2020-218644

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      We read with interest the correspondence from Mizugishi et al.1 The pathophysiology of Kawasaki disease (KD) and more recently Kawasaki-like paediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2 (PIMS-TS) or Kawa-COVID-19 remains largely unknown, even if the infectious trigger by SARS-CoV-2 in the prior weeks seems to be a key feature.2 Furthermore, it is still uncertain whether Kawasaki-like PIMS-TS can be considered as the same entity as KD or if it should be individualised as a novel distinct condition, as it may have been suggested with several significant clinical and biological differences between classical KD and Kawa-COVID-19.3

      Mizugishi et al 1 speculate that KD and Kawa-COVID-19 share a common pathophysiology through excessive neutrophil extracellular trap (NET) formation. Similar to Yoshida et al,4 Mizugishi et al 1 showed increased NET formation in KD patients sera. Through a KD mouse model, the authors describe that severe vasculitis (in the aorta and coronary arteries) was associated with infiltrative neutrophils. Those neutrophils were primed to produce NETs through the PAD4 pathway and seemed to produce a specific type of NET formation (enriched in citrullinated histones). Excessive NET formation was also described in sera of adult COVID-19 patients with endothelial injuries. Kawa-COVID-19 could represent a severe form of KD triggered by an exaggerated NET formation induced by SARS-CoV-2.

      NETs are an important first-line defence mechanism against bacterial, viral, fungal and parasitic infections, but they have been also suspected to play a role in autoimmune diseases such as systemic lupus erythematosus (SLE) or antineutrophil cytoplasmic antibodies-associated vasculitis (AAV) for example.5 Van Dam et al 5 showed that NET formation is involved in the pathophysiology of two clinically and pathologically distinct forms …

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