Microglia lacking a peroxisomal β-oxidation enzyme chronically alter their inflammatory profile without evoking neuronal and behavioral deficits.


Journal

Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974

Informations de publication

Date de publication:
13 Mar 2019
Historique:
received: 11 12 2018
accepted: 24 02 2019
entrez: 15 3 2019
pubmed: 15 3 2019
medline: 16 7 2019
Statut: epublish

Résumé

Microglia play a central role in most neurological disorders, but the impact of microgliosis on brain environment and clinical functions is not fully understood. Mice lacking multifunctional protein-2 (MFP2), a pivotal enzyme in peroxisomal β-oxidation, develop a fatal disorder characterized by motor problems similar to the milder form of MFP2 deficiency in humans. The hallmark of disease in mice is the chronic proliferation of microglia in the brain, but molecular pathomechanisms that drive rapid clinical deterioration in human and mice remain unknown. In the present study, we identified the effects of specific deletion of MFP2 from microglia in the brain on immune responses, neuronal functioning, and behavior. We created a novel Cx3cr1-Mfp2 We found that Mfp2 Our data demonstrate that MFP2 deficiency in microglia causes intrinsic dysregulation of their inflammatory profile, which is not harmful to neuronal function, motor function, and cognition in mice during their first year of life.

Sections du résumé

BACKGROUND BACKGROUND
Microglia play a central role in most neurological disorders, but the impact of microgliosis on brain environment and clinical functions is not fully understood. Mice lacking multifunctional protein-2 (MFP2), a pivotal enzyme in peroxisomal β-oxidation, develop a fatal disorder characterized by motor problems similar to the milder form of MFP2 deficiency in humans. The hallmark of disease in mice is the chronic proliferation of microglia in the brain, but molecular pathomechanisms that drive rapid clinical deterioration in human and mice remain unknown. In the present study, we identified the effects of specific deletion of MFP2 from microglia in the brain on immune responses, neuronal functioning, and behavior.
METHODS METHODS
We created a novel Cx3cr1-Mfp2
RESULTS RESULTS
We found that Mfp2
CONCLUSION CONCLUSIONS
Our data demonstrate that MFP2 deficiency in microglia causes intrinsic dysregulation of their inflammatory profile, which is not harmful to neuronal function, motor function, and cognition in mice during their first year of life.

Identifiants

pubmed: 30866963
doi: 10.1186/s12974-019-1442-3
pii: 10.1186/s12974-019-1442-3
pmc: PMC6417251
doi:

Substances chimiques

Aif1 protein, mouse 0
CX3C Chemokine Receptor 1 0
Calcium-Binding Proteins 0
Cx3cr1 protein, mouse 0
Lipopolysaccharides 0
Microfilament Proteins 0
Interleukin-4 207137-56-2
Hsd17b4 protein, mouse EC 1.1.1.119
Peroxisomal Multifunctional Protein-2 EC 4.2.1.107

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

61

Subventions

Organisme : Vlaamse regering
ID : G.0675.12
Organisme : Vlaamse regering
ID : G.0A15.13
Organisme : Onderzoeksraad, KU Leuven
ID : OT12/78

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Auteurs

Lien Beckers (L)

Department of Pharmaceutical and Pharmacological Sciences, Laboratory for Cell Metabolism, KU Leuven - University of Leuven, Campus Gasthuisberg O/N2, Herestraat 49, B-3000, Leuven, Belgium.
Present Address: Center for Translational and Computational Neuro-immunology, Department of Neurology, Columbia University Medical Center, New York City, NY, USA.

Ivana Geric (I)

Department of Pharmaceutical and Pharmacological Sciences, Laboratory for Cell Metabolism, KU Leuven - University of Leuven, Campus Gasthuisberg O/N2, Herestraat 49, B-3000, Leuven, Belgium.

Stijn Stroobants (S)

Faculty of Psychology and Educational Sciences, Biological Psychology Unit, KU Leuven - University of Leuven, B-3000, Leuven, Belgium.

Sander Beel (S)

Department of Neurosciences, Laboratory for Neurobiology, KU Leuven - University of Leuven, Leuven, Belgium.
Center for Brain and Disease Research, VIB, Leuven, Belgium.

Philip Van Damme (P)

Department of Neurosciences, Laboratory for Neurobiology, KU Leuven - University of Leuven, Leuven, Belgium.
Center for Brain and Disease Research, VIB, Leuven, Belgium.
Neurology Department, University Hospitals Leuven, Leuven, Belgium.

Rudi D'Hooge (R)

Faculty of Psychology and Educational Sciences, Biological Psychology Unit, KU Leuven - University of Leuven, B-3000, Leuven, Belgium.

Myriam Baes (M)

Department of Pharmaceutical and Pharmacological Sciences, Laboratory for Cell Metabolism, KU Leuven - University of Leuven, Campus Gasthuisberg O/N2, Herestraat 49, B-3000, Leuven, Belgium. Myriam.Baes@kuleuven.be.

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Classifications MeSH