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The difference of the inflammatory milieu in MIS-C and severe COVID-19

Sibel Lacinel Gurlevik1, Yasemin Ozsurekci1, Erdal Sağ2,3

  • 1Department of Pediatric Infectious Diseases, Faculty of Medicine, Hacettepe University, Ankara, Turkey.

Pediatric Research
|March 30, 2022
PubMed

Insights

Multisystem inflammatory syndrome in children (MIS-C) involves distinct immune responses, particularly involving IL-1 and IFN-γ pathways. Understanding these cytokine profiles helps in managing post-COVID complications in children.

Area of Science:

  • Pediatric Immunology
  • Infectious Diseases
  • Cytokine Signaling

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause severe illness in children.
  • Multisystem inflammatory syndrome in children (MIS-C) is a post-COVID-19 complication characterized by heightened inflammation.
  • Limited data exists on the specific immunological mechanisms driving MIS-C.

Purpose of the Study:

  • To investigate the cytokine and chemokine profiles in children diagnosed with MIS-C.
  • To compare these profiles with those of children experiencing severe/critical COVID-19 and healthy controls.
  • To elucidate the underlying pathophysiology of MIS-C.

Main Methods:

  • Analysis of cytokine and chemokine profiles in blood samples.
  • Comparison of immune profiles across three groups: MIS-C patients, severe/critical COVID-19 patients, and healthy controls.
  • Study included 31 MIS-C patients, 10 severe/critical COVID-19 patients, and 11 healthy controls.

Main Results:

  • Children with MIS-C exhibited significantly elevated levels of IL-1 family cytokines, IFN-γ pathway related chemokines (including IL-18 and MIG/CXCL9), and IL-17A compared to severe/critical COVID-19 and healthy controls.
  • IP-10/CXCL10 and IL-10 were found to be elevated in both MIS-C and severe/critical COVID-19 groups relative to healthy controls.
  • Distinct patterns of immune activation were identified for MIS-C and severe COVID-19.

Conclusions:

  • The IL-1 and IFN-γ pathways are implicated as key players in the pathophysiology of MIS-C.
  • Identifying specific immune response patterns can aid in understanding MIS-C.
  • Further research may lead to biomarkers for early identification and management of MIS-C risk in children.
Abstract

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