Impaired peroxisomal beta-oxidation in microglia triggers oxidative stress and impacts neurons and oligodendrocytes
Open accessAbstract
Microglia, the immune cells of the central nervous system, activate neuroinflammatory pathways in response to homeostatic disturbances, a process implicated in the pathogenesis of various neurodegenerative diseases. Emerging evidence identifies abnormal microglial activation as a causal factor at the onset of peroxisomal leukodystrophies, including X-linked adrenoleukodystrophy (X-ALD). This study investigates how primary peroxisomal deficiencies influence oxidative properties of microglia and examines the subsequent impact on neurons and oligodendrocytes. Using BV-2 microglial cells lacking ABCD1, ABCD2, or ACOX1, peroxisomal proteins that play key roles in the very-long-chain fatty acid beta-oxidation, we analyzed their response under basal condition and after stimulation by lipopolysaccharide (LPS). Transcriptomic analysis of the mutant microglial cells revealed numerous differentially expressed genes, particularly in redox-related pathways following LPS exposure. These changes are consistent with the increased production of reactive oxygen species (ROS) and nitric oxide (NO). Conditioned media (CM) from the mutant cells were then applied to cultures of neuron and oligodendrocyte cell lines. Exposure to CM from LPS-stimulated mutant microglial cells significantly increased apoptosis in both cell types. Furthermore, treated neurons exhibited a reduction in cell complexity and an increased ability to secrete neuropeptides. These findings demonstrate that peroxisomal impairments in microglia exacerbate inflammatory response and ROS/NO production, affecting the survival of neurons and oligodendrocytes, as well as neuronal morphology and function. This dysfunction might contribute to the early neurodegenerative events in X-ALD by triggering and sustaining neuroinflammatory cascades. Therapeutic strategies that target microglial activation and secretion profiles could hold promise in managing peroxisomal disorders such as X-ALD.
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Following LPS exposure, ABCD1-mutated microglia had numerous differentially expressed genes encoding pro-inflammatory cytokines or involved in phagocytosis, antigen presentation, and co-stimulation of T lymphocytes.
“Following LPS exposure, the ABCD1-mutated microglia had numerous differentially expressed genes encoding pro-inflammatory cytokines or involved in phagocytosis, antigen presentation, and co-stimulation of T lymphocytes.”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [351]
The Results section reports numerous differentially expressed genes in LPS-treated mutant BV-2 microglia, but this paper’s gene analysis focuses on redox-related genes. The Discussion reports an amplified inflammatory response and changes in phagocytosis and antigen presentation; it does not establish that the reported DEGs encode pro-inflammatory cytokines or are involved in those functions or T-lymphocyte co-stimulation. No page numbers are available in our copy. (LLM, conf=0.86)
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EFEITO GLICOTÓXICO EM CÉLULAS DA MICRÓGLIA (BV-2)
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Self-citation
- Authors
- Tawbeh, A., Gondcaille, C., Saih, F.-E., Raas, Q., Loichot, D., Hamon, Y., Keime, C., Benani, A., Di Cara, F., Cherkaoui-Malki, M., Andreoletti, P., & Savary, S.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Savary, Stéphane
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2025-01-30
- Volume
- 18
- Pages
- 1542938-1542938
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC11826809
- OpenAlex
- W4407002105
- Cited by
- 21
- References
- 84
- Citations by year
- 2026: 14 · 2025: 7
- FWCI
- 7.58
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Aix-Marseille Université
- Agence Nationale de la Recherche (ANR-17-CE15-0032)
- Institut National de la Santé et de la Recherche Médicale
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- microglia, peroxisomal beta-oxidation, X-linked adrenoleukodystrophy, peroxisomal disorders, oxidative stress, reactive oxygen species, nitric oxide, ABCD1, ABCD2, ACOX1, very long chain fatty acids, lipopolysaccharide, neuroinflammation, neuronal apoptosis, oligodendrocytes, conditioned medium, neuropeptide release, neuronal morphology, neurodegeneration
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