Immunoprofiling of active and inactive systemic juvenile idiopathic arthritis reveals distinct biomarkers: a single-center study.

Cytokines and inflammatory mediators High mobility group Box 1 Inflammation Ingenuity pathway analysis Proteomics Systemic juvenile idiopathic arthritis

Journal

Pediatric rheumatology online journal
ISSN: 1546-0096
Titre abrégé: Pediatr Rheumatol Online J
Pays: England
ID NLM: 101248897

Informations de publication

Date de publication:
28 Dec 2021
Historique:
received: 06 10 2021
accepted: 15 12 2021
entrez: 29 12 2021
pubmed: 30 12 2021
medline: 4 2 2022
Statut: epublish

Résumé

This study aimed to perform an immunoprofiling of systemic juvenile idiopathic arthritis (sJIA) in order to define biomarkers of clinical use as well as reveal new immune mechanisms. Immunoprofiling of plasma samples from a clinically well-described cohort consisting of 21 sJIA patients as well as 60 age and sex matched healthy controls, was performed by a highly sensitive proteomic immunoassay. Based on the biomarkers being significantly up- or down-regulated in cross-sectional and paired analysis, related canonical pathways and cellular functions were explored by Ingenuity Pathway Analysis (IPA). The well-studied sJIA biomarkers, IL6, IL18 and S100A12, were confirmed to be increased during active sJIA as compared to healthy controls. IL18 was the only factor found to be increased during inactive sJIA as compared to healthy controls. Novel factors, including CASP8, CCL23, CD6, CXCL1, CXCL11, CXCL5, EIF4EBP1, KITLG, MMP1, OSM, SIRT2, SULT1A1 and TNFSF11, were found to be differentially expressed in active and/or inactive sJIA and healthy controls. No significant pathway activation could be predicted based on the limited factor input to the IPA. High Mobility Group Box 1 (HMGB1), a damage associated molecular pattern being involved in a series of inflammatory diseases, was determined to be higher in active sJIA than inactive sJIA. We could identify a novel set of biomarkers distinguishing active sJIA from inactive sJIA or healthy controls. Our findings enable a better understanding of the immune mechanisms active in sJIA and aid the development of future diagnostic and therapeutic strategies.

Sections du résumé

BACKGROUND BACKGROUND
This study aimed to perform an immunoprofiling of systemic juvenile idiopathic arthritis (sJIA) in order to define biomarkers of clinical use as well as reveal new immune mechanisms.
METHODS METHODS
Immunoprofiling of plasma samples from a clinically well-described cohort consisting of 21 sJIA patients as well as 60 age and sex matched healthy controls, was performed by a highly sensitive proteomic immunoassay. Based on the biomarkers being significantly up- or down-regulated in cross-sectional and paired analysis, related canonical pathways and cellular functions were explored by Ingenuity Pathway Analysis (IPA).
RESULTS RESULTS
The well-studied sJIA biomarkers, IL6, IL18 and S100A12, were confirmed to be increased during active sJIA as compared to healthy controls. IL18 was the only factor found to be increased during inactive sJIA as compared to healthy controls. Novel factors, including CASP8, CCL23, CD6, CXCL1, CXCL11, CXCL5, EIF4EBP1, KITLG, MMP1, OSM, SIRT2, SULT1A1 and TNFSF11, were found to be differentially expressed in active and/or inactive sJIA and healthy controls. No significant pathway activation could be predicted based on the limited factor input to the IPA. High Mobility Group Box 1 (HMGB1), a damage associated molecular pattern being involved in a series of inflammatory diseases, was determined to be higher in active sJIA than inactive sJIA.
CONCLUSIONS CONCLUSIONS
We could identify a novel set of biomarkers distinguishing active sJIA from inactive sJIA or healthy controls. Our findings enable a better understanding of the immune mechanisms active in sJIA and aid the development of future diagnostic and therapeutic strategies.

Identifiants

pubmed: 34963488
doi: 10.1186/s12969-021-00660-9
pii: 10.1186/s12969-021-00660-9
pmc: PMC8713412
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

173

Subventions

Organisme : Karolinska Institutet
ID : KIK2HEH
Organisme : Vetenskapsrådet
ID : 2018-02885
Organisme : region Stockholm
ID : 20190592
Organisme : China Scholarship Council
ID : 201807930002

Informations de copyright

© 2021. The Author(s).

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Auteurs

Heshuang Qu (H)

Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Division of Rheumatology, Karolinska University Hospital, Stockholm, Sweden.

Erik Sundberg (E)

Unit of Pediatric Rheumatology, Karolinska University Hospital, Stockholm, Sweden.
Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.

Cecilia Aulin (C)

Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Division of Rheumatology, Karolinska University Hospital, Stockholm, Sweden.

Manoj Neog (M)

Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Division of Rheumatology, Karolinska University Hospital, Stockholm, Sweden.

Karin Palmblad (K)

Unit of Pediatric Rheumatology, Karolinska University Hospital, Stockholm, Sweden.
Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.

Anna Carin Horne (AC)

Unit of Pediatric Rheumatology, Karolinska University Hospital, Stockholm, Sweden.
Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.

Fredrik Granath (F)

Division of Clinical Epidemiology, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.

Alexandra Ek (A)

Center for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden.

Erik Melén (E)

Sachs Children's Hospital, Stockholm, Sweden.
Department of Clinical Sciences and Education, Karolinska Institutet, Södersjukhuset, Stockholm, Sweden.

Mia Olsson (M)

Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Division of Rheumatology, Karolinska University Hospital, Stockholm, Sweden.

Helena Erlandsson Harris (HE)

Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. helena.harris@ki.se.
Division of Rheumatology, Karolinska University Hospital, Stockholm, Sweden. helena.harris@ki.se.

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Classifications MeSH