CHIT1 at diagnosis predicts faster disability progression and reflects early microglial activation in multiple sclerosis.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
12 Jun 2024
Historique:
received: 09 11 2023
accepted: 30 05 2024
medline: 13 6 2024
pubmed: 13 6 2024
entrez: 12 6 2024
Statut: epublish

Résumé

Multiple sclerosis (MS) is characterized by heterogeneity in disease course and prediction of long-term outcome remains a major challenge. Here, we investigate five myeloid markers - CHIT1, CHI3L1, sTREM2, GPNMB and CCL18 - in the cerebrospinal fluid (CSF) at diagnostic lumbar puncture in a longitudinal cohort of 192 MS patients. Through mixed-effects and machine learning models, we show that CHIT1 is a robust predictor for faster disability progression. Integrative analysis of 11 CSF and 26 central nervous system (CNS) parenchyma single-cell/nucleus RNA sequencing samples reveals CHIT1 to be predominantly expressed by microglia located in active MS lesions and enriched for lipid metabolism pathways. Furthermore, we find CHIT1 expression to accompany the transition from a homeostatic towards a more activated, MS-associated cell state in microglia. Neuropathological evaluation in post-mortem tissue from 12 MS patients confirms CHIT1 production by lipid-laden phagocytes in actively demyelinating lesions, already in early disease stages. Altogether, we provide a rationale for CHIT1 as an early biomarker for faster disability progression in MS.

Identifiants

pubmed: 38866782
doi: 10.1038/s41467-024-49312-y
pii: 10.1038/s41467-024-49312-y
doi:

Substances chimiques

Biomarkers 0
chitotriosidase EC 3.2.1.-
Hexosaminidases EC 3.2.1.-
Chitinase-3-Like Protein 1 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

5013

Subventions

Organisme : KU Leuven (Katholieke Universiteit Leuven)
ID : BOF-FKO
Organisme : National Multiple Sclerosis Society (National MS Society)
ID : PA-2002-36277
Organisme : Fonds Wetenschappelijk Onderzoek (Research Foundation Flanders)
ID : 11A0523N
Organisme : Fonds Wetenschappelijk Onderzoek (Research Foundation Flanders)
ID : 1S38023N

Informations de copyright

© 2024. The Author(s).

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Auteurs

Jarne Beliën (J)

Laboratory for Neuroimmunology, Department of Neurosciences, Leuven Brain Institute, KU Leuven, Leuven, Belgium.

Stijn Swinnen (S)

Laboratory for Neuroimmunology, Department of Neurosciences, Leuven Brain Institute, KU Leuven, Leuven, Belgium.
Department of Neurology, University Hospitals Leuven, Leuven, Belgium.

Robbe D'hondt (R)

Department of Public Health and Primary Care, KU Leuven, Kortrijk, Belgium.
Imec research group itec, KU Leuven, Kortrijk, Belgium.

Laia Verdú de Juan (LV)

Department of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.

Nina Dedoncker (N)

Laboratory for Neuroimmunology, Department of Neurosciences, Leuven Brain Institute, KU Leuven, Leuven, Belgium.

Patrick Matthys (P)

Laboratory of Immunobiology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium.

Jan Bauer (J)

Department of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.

Celine Vens (C)

Department of Public Health and Primary Care, KU Leuven, Kortrijk, Belgium.
Imec research group itec, KU Leuven, Kortrijk, Belgium.

Sinéad Moylett (S)

Laboratory for Neuroimmunology, Department of Neurosciences, Leuven Brain Institute, KU Leuven, Leuven, Belgium.

Bénédicte Dubois (B)

Laboratory for Neuroimmunology, Department of Neurosciences, Leuven Brain Institute, KU Leuven, Leuven, Belgium. benedicte.dubois@uzleuven.be.
Department of Neurology, University Hospitals Leuven, Leuven, Belgium. benedicte.dubois@uzleuven.be.

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