Lipocalin-2 does not influence EAE clinical score but it increases inflammation in central nervous system.
Demyelination
Experimental autoimmune encephalomyelitis
Immunomodulation
Lipocalin-2
Multiple sclerosis
Journal
Journal of neuroimmunology
ISSN: 1872-8421
Titre abrégé: J Neuroimmunol
Pays: Netherlands
ID NLM: 8109498
Informations de publication
Date de publication:
15 07 2022
15 07 2022
Historique:
received:
06
12
2021
revised:
05
04
2022
accepted:
13
04
2022
pubmed:
4
5
2022
medline:
10
6
2022
entrez:
3
5
2022
Statut:
ppublish
Résumé
The contribution of lipocalin-2 (LCN2) to multiple sclerosis (MS) is controversial. Herein, we induced experimental autoimmune encephalomyelitis (EAE) in LCN2-null and wild-type (Wt) mice. While we did not find differences between genotypes regarding clinical score, LCN2-null EAE mice presented decreased expression of interferon gamma and diminished demyelination in the cerebellum. Both genotypes presented similar alterations in the thymocyte and splenocyte populations. In MS patients, higher LCN2 CSF levels at diagnosis could be associated with faster disease progression, however further studies are needed to confirm these results, since this association was lost after controlling for the patients age, presence of oligoclonal bands and gender. Overall, our results support a harmful role for LCN2 in the disease context.
Identifiants
pubmed: 35504189
pii: S0165-5728(22)00067-4
doi: 10.1016/j.jneuroim.2022.577872
pii:
doi:
Substances chimiques
LCN2 protein, human
0
Lipocalin-2
0
Lcn2 protein, mouse
126469-30-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
577872Informations de copyright
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