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Pericytes: The Brain's Very First Responders?
Victoria A Rafalski1, Mario Merlini1, Katerina Akassoglou2
1Gladstone Institutes, San Francisco, CA 94158, USA.
Neuron
|October 12, 2018
Summary
Systemic infection triggers specific neurovascular cells to release the chemokine CCL2. This rapid response increases neural excitability, impacting brain function.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Infections can impair cognitive and neural functions.
- The neurovascular unit plays a critical role in brain homeostasis and response to stimuli.
Purpose of the Study:
- To investigate the cellular mechanisms by which infection impacts neural function.
- To identify specific cell types and molecular mediators involved in the brain's response to systemic infection.
Main Methods:
- Utilized mouse models of systemic infection.
- Investigated the expression and release of chemokines from neurovascular unit cells.
- Assessed changes in neural excitability following infection.
Main Results:
- Identified platelet-derived growth factor receptor beta (PDGFRβ)-expressing cell subtypes within the neurovascular unit.
- Demonstrated rapid release of chemokine (C-C motif) ligand 2 (CCL2) from these cells post-infection.
- Showed that CCL2 release leads to increased neural excitability.
Conclusions:
- Specific PDGFRβ-expressing cells in the neurovascular unit are key responders to systemic infection.
- CCL2 is a critical mediator linking infection to altered neural activity.
- These findings highlight a mechanism for infection-induced neuroinflammation and functional deficits.