Inflammatory responses in SARS-CoV-2 associated Multisystem Inflammatory Syndrome and Kawasaki Disease in children: An observational study

G. Biesbroek*, B. Kapitein, I. M. Kuipers, M. P. Gruppen, D. van Stijn, T. E. Peros, M. van Veenendaal, M. H.A. Jansen, C. W. van der Zee, M. van der Kuip, E. G.J. von Asmuth, M. G. Mooij, M. E.J. den Boer, G. W. Landman, M. A. van Houten, D. Schonenberg-Meinema, A. M. Tutu van Furth, M. Boele van Hensbroek, H. Scherpbier, K. E. van MeijgaardenT. H.M. Ottenhoff, S. A. Joosten, N. Ketharanathan, M. Blink, C. L.H. Brackel, H. L. Zaaijer, P. Hombrink, J. M. van den Berg, E. P. Buddingh, T. W. Kuijpers

*Corresponding author for this work

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Abstract

Multisystem Inflammatory Syndrome in Children (MIS-C) is a severe inflammatory disease in children related to SARS-CoV-2 with multisystem involvement including marked cardiac dysfunction and clinical symptoms that can resemble Kawasaki Disease (KD). We hypothesized that MIS-C and KD might have commonalities as well as unique inflammatory responses and studied these responses in both diseases. In total, fourteen children with MIS-C (n=8) and KD (n=6) were included in the period of March-June 2020. Clinical and routine blood parameters, cardiac follow-up, SARS-CoV-2-specific antibodies and CD4+ T-cell responses, and cytokine-profiles were determined in both groups. In contrast to KD patients, all MIS-C patients had positive Spike protein-specific CD3+CD4+ T-cell responses. MIS-C and KD patients displayed marked hyper-inflammation with high expression of serum cytokines, including the drug-targetable interleukin (IL)-6 and IFN-γ associated chemokines CXCL9, 10 and 11, which decreased at follow-up. No statistical differences were observed between groups. Clinical outcomes were all favourable without cardiac sequelae at 6 months follow-up. In conclusion, MIS-C and KD-patients both displayed cytokine-associated hyper-inflammation with several high levels of drug-targetable cytokines.

Original languageEnglish
Article numbere0266336
JournalPLoS ONE
Volume17
Issue number11 November
DOIs
Publication statusPublished - 30 Nov 2022

Bibliographical note

Funding acquisition: E. P. Buddingh, T. W. Kuijpers.

Publisher Copyright:
Copyright: © 2022 Biesbroek et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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