Long-term cytokine profile in multisystem inflammatory disease among children.

COVID-19 Children Complications Cytokines Long-term follow-up Multisystem inflammatory disease

Journal

Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353

Informations de publication

Date de publication:
27 Aug 2024
Historique:
received: 10 03 2024
revised: 19 08 2024
accepted: 22 08 2024
medline: 31 8 2024
pubmed: 31 8 2024
entrez: 29 8 2024
Statut: aheadofprint

Résumé

Multisystem inflammatory disease in children (MIS-C) is a post-infectious condition following coronavirus disease-19 infection. Long-term follow-up data suggests that initial clinical severity does not necessarily correlate with long-term outcomes. The long-term immunological response in children with MIS-C remains poorly understood. We analyzed cytokine profiles at diagnosis and during follow-up, in pediatric patients with MIS-C, exploring correlations among cytokine expressions and standard biochemical and hormonal test results. Twenty-five MIS-C patients (mean 9.4 ± 3.9) with complete test results at diagnosis and at 6- and 12-months follow-up were included in the study. Selected cytokines, such as IL-9, eotaxin, IP-10, MIP-1β, RANTES, MCP-1(MCAF), TNF-α, PDGF-B, IL-4, and MIP-1α, were included in the analysis. IP-10, MCP-1 (MCAF), and MIP-1α levels normalized or nearly normalized at 6-12 months, the remaining cytokines, including IL-9, eotaxin, MIP-1β, RANTES, TNF-α, PDGF-B, IL-4, remained higher in MIS-C than in controls at our last follow-up time. At 6 months post-diagnosis, a mild negative correlation between triglycerides and HOMA-IR with MCP-1 (MCAF), IL-4, and Eotaxin was noted. At the 12-month follow-up we found a mild positive correlation of cortisol and ACTH levels with PDGF-B, MIP-1α, and TNF-α. Conversely, a negative correlation between these cytokines with fasting glucose and HOMA-IR was observed. Our study findings highlight a notable cytokine-mediated inflammatory response in pediatric patients with MIS-C, characterized by sustained elevated levels over a 12-month monitoring period compared to the control group. We have identified various interrelationships among different cytokines, as well as correlations between heightened cytokine levels and metabolic and hormonal patterns. The pronounced inflammatory response underscores its involvement in acute organ damage, while its persistence suggests potential implications for long-term metabolic disorders.

Sections du résumé

BACKGROUND BACKGROUND
Multisystem inflammatory disease in children (MIS-C) is a post-infectious condition following coronavirus disease-19 infection. Long-term follow-up data suggests that initial clinical severity does not necessarily correlate with long-term outcomes. The long-term immunological response in children with MIS-C remains poorly understood. We analyzed cytokine profiles at diagnosis and during follow-up, in pediatric patients with MIS-C, exploring correlations among cytokine expressions and standard biochemical and hormonal test results.
METHODS METHODS
Twenty-five MIS-C patients (mean 9.4 ± 3.9) with complete test results at diagnosis and at 6- and 12-months follow-up were included in the study. Selected cytokines, such as IL-9, eotaxin, IP-10, MIP-1β, RANTES, MCP-1(MCAF), TNF-α, PDGF-B, IL-4, and MIP-1α, were included in the analysis.
RESULTS RESULTS
IP-10, MCP-1 (MCAF), and MIP-1α levels normalized or nearly normalized at 6-12 months, the remaining cytokines, including IL-9, eotaxin, MIP-1β, RANTES, TNF-α, PDGF-B, IL-4, remained higher in MIS-C than in controls at our last follow-up time. At 6 months post-diagnosis, a mild negative correlation between triglycerides and HOMA-IR with MCP-1 (MCAF), IL-4, and Eotaxin was noted. At the 12-month follow-up we found a mild positive correlation of cortisol and ACTH levels with PDGF-B, MIP-1α, and TNF-α. Conversely, a negative correlation between these cytokines with fasting glucose and HOMA-IR was observed.
CONCLUSIONS CONCLUSIONS
Our study findings highlight a notable cytokine-mediated inflammatory response in pediatric patients with MIS-C, characterized by sustained elevated levels over a 12-month monitoring period compared to the control group. We have identified various interrelationships among different cytokines, as well as correlations between heightened cytokine levels and metabolic and hormonal patterns. The pronounced inflammatory response underscores its involvement in acute organ damage, while its persistence suggests potential implications for long-term metabolic disorders.

Identifiants

pubmed: 39205361
pii: S1043-4666(24)00247-3
doi: 10.1016/j.cyto.2024.156744
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

156744

Informations de copyright

Copyright © 2024 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Valeria Calcaterra (V)

Department of Internal Medicine and Therapeutics, University of Pavia, Pavia, Italy; Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Cristian Loretelli (C)

International Center for T1D, Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Science, Università di Milano, Milano, Italy.

Davide Biganzoli (D)

Center of Functional Genomics and Rare Diseases, Buzzi Children's Hospital, Milano, Italy.

Ahmed Abdelsalam (A)

International Center for T1D, Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Science, Università di Milano, Milano, Italy.

Giuseppe Marano (G)

Medical Statistics Unit, Department of Biomedical and Clinical Sciences, "Luigi Sacco" University Hospital, University of Milano, Data Science Research Center, Milano, Italy.

Stephana Carelli (S)

Center of Functional Genomics and Rare Diseases, Buzzi Children's Hospital, Milano, Italy.

Laura Fiori (L)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Savina Mannarino (S)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Enza D'Auria (E)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Elvira Verduci (E)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Raffaella De Santis (R)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Dario Dilillo (D)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Valentina Fabiano (V)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy; Department of Biomedical and Clinical Sciences, University of Milano, Milano, Italy. Electronic address: valentina.fabiano@unimi.it.

Patrizia Carlucci (P)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy.

Erika Maghraby (E)

Center of Functional Genomics and Rare Diseases, Buzzi Children's Hospital, Milano, Italy; Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, University of Milano, Milano, Italy; Department of Biology and Biotechnology "L. Spallanzani" (DBB), University of Pavia, Pavia, Italy; Division of Endocrinology, ASST Fatebenefratelli-Sacco, Milano, Italy.

Letizia Messa (L)

Center of Functional Genomics and Rare Diseases, Buzzi Children's Hospital, Milano, Italy.

Cristina Cereda (C)

Center of Functional Genomics and Rare Diseases, Buzzi Children's Hospital, Milano, Italy.

Paolo Fiorina (P)

International Center for T1D, Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Science, Università di Milano, Milano, Italy.

Elia Biganzoli (E)

Medical Statistics Unit, Department of Biomedical and Clinical Sciences, "Luigi Sacco" University Hospital, University of Milano, Data Science Research Center, Milano, Italy.

Gianvincenzo Zuccotti (G)

Pediatric Department, Buzzi Children's Hospital, Milano, Italy; Department of Biomedical and Clinical Sciences, University of Milano, Milano, Italy.

Classifications MeSH