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Acute neuroinflammation promotes a metabolic shift that alters extracellular vesicle cargo in the mouse brain cortex
Natasha Vassileff1,2,3, Jereme G Spiers1,2,3, Juliani Juliani1,4,5
1The Department of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe Institute for Molecular Science La Trobe University Bundoora Victoria Australia.
Abstract:
Neuroinflammation is initiated through microglial activation and cytokine release which can be induced through lipopolysaccharide treatment (LPS) leading to a transcriptional cascade culminating in the differential expression of target proteins. These differentially expressed proteins can then be packaged into extracellular vesicles (EVs), a form of cellular communication, further propagating the neuroinflammatory response over long distances. Despite this, the EV proteome in the brain, following LPS treatment, has not been investigated. Brain tissue and brain derived EVs (BDEVs) isolated from the cortex of LPS-treated mice underwent thorough characterisation to meet the minimal information for studies of extracellular vesicles guidelines before undergoing mass spectrometry analysis to identify the differentially expressed proteins. Fourteen differentially expressed proteins were identified in the LPS brain tissue samples compared to the controls and 57 were identified in the BDEVs isolated from the LPS treated mice compared to the controls. This included proteins associated with the initiation of the inflammatory response, epigenetic regulation, and metabolism. These results allude to a potential link between small EV cargo and early inflammatory signalling.
Insights
Lipopolysaccharide (LPS) treatment activates brain microglial cells, leading to neuroinflammation. Researchers identified specific proteins in brain-derived extracellular vesicles (EVs) that may propagate this inflammatory response.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Neuroinflammation, triggered by microglial activation and cytokine release, is a key pathological process.
- Lipopolysaccharide (LPS) is a common inducer of experimental neuroinflammation.
- Extracellular vesicles (EVs) mediate cell-to-cell communication and can propagate inflammatory signals.
Purpose of the Study:
- To investigate the proteomic changes in brain-derived extracellular vesicles (BDEVs) following LPS treatment.
- To identify proteins within BDEVs that may contribute to the propagation of neuroinflammation.
Main Methods:
- Mice were treated with LPS to induce neuroinflammation.
- Brain tissue and BDEVs were isolated from the cortex.
- Proteomic analysis using mass spectrometry was performed on both brain tissue and BDEVs.
- EV characterization followed the Minimal Information for Studies of Extracellular Vesicles guidelines.
Main Results:
- Fourteen differentially expressed proteins were identified in LPS-treated brain tissue compared to controls.
- Fifty-seven differentially expressed proteins were identified in BDEVs from LPS-treated mice compared to controls.
- These proteins were associated with inflammation initiation, epigenetic regulation, and metabolism.
Conclusions:
- LPS treatment induces significant proteomic alterations in both brain tissue and BDEVs.
- The cargo of BDEVs includes proteins involved in inflammatory signaling, suggesting a role in propagating neuroinflammation.
- This study highlights a potential link between EV protein content and early inflammatory responses in the brain.
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