Commentary 10.1172/JCI151467

Zonulin as a biomarker and potential therapeutic target in multisystem inflammatory syndrome in children

Tiffany Hensley-McBain1 and Jennifer A. Manuzak2

1Clinical Care Options, Reston, Virginia, USA.

2Division of Immunology, Tulane National Primate Research Center, Tulane University, Covington, Louisiana, USA.

Address correspondence to: Jennifer A. Manuzak, Tulane National Primate Research Center, 18703 Three Rivers Road, Covington, Louisiana 70433, USA. Phone: 985.871.6473; Email: jmanuzak@tulane.edu.

Find articles by Hensley-McBain, T. in: JCI | PubMed | Google Scholar

1Clinical Care Options, Reston, Virginia, USA.

2Division of Immunology, Tulane National Primate Research Center, Tulane University, Covington, Louisiana, USA.

Address correspondence to: Jennifer A. Manuzak, Tulane National Primate Research Center, 18703 Three Rivers Road, Covington, Louisiana 70433, USA. Phone: 985.871.6473; Email: jmanuzak@tulane.edu.

Find articles by Manuzak, J. in: JCI | PubMed | Google Scholar |

Published June 23, 2021 - More info

Published in Volume 131, Issue 14 on July 15, 2021
J Clin Invest. 2021;131(14):e151467. https://doi.org/10.1172/JCI151467.
© 2021 American Society for Clinical Investigation
Published June 23, 2021 - Version history
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Multisystem inflammatory syndrome in children (MIS-C) occurs during or recently following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and is characterized by persistent fever, inflammation, and severe illness requiring hospitalization. The majority of patients with MIS-C also present with gastrointestinal (GI) symptoms, including abdominal pain, vomiting, and diarrhea. In this issue of the JCI, Yonker, Gilboa, and colleagues identified zonulin as a biomarker of GI permeability in children with MIS-C and present the results of an intriguing proof-of-concept study indicating that zonulin may represent a potential therapeutic target for MIS-C treatment and prevention. Their findings suggest that intestinal mucosal dysfunction and epithelial barrier breakdown may represent a biological mechanism underlying the development of MIS-C in SARS-CoV-2–infected children.

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