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Microglial-derived microparticles mediate neuroinflammation after traumatic brain injury
Alok Kumar1,2, Bogdan A Stoica1,2, David J Loane1,2
1Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA.
Journal of Neuroinflammation
|March 16, 2017
Summary
Microparticles (MPs) released after traumatic brain injury (TBI) spread neuroinflammation by activating brain immune cells. These MPs can initiate inflammatory responses, offering a potential therapeutic target for neurological disorders.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Traumatic brain injury (TBI) triggers early local and systemic inflammatory responses, contributing to secondary injury and neurological deficits.
- The precise mechanisms driving rapid neuroinflammation expansion and long-term progression post-TBI remain unclear.
- Microparticles (MPs), a type of extracellular vesicle, are investigated for their role in propagating inflammation after brain trauma.
Purpose of the Study:
- To investigate the role of microparticles (MPs) in the exchange of pro-inflammatory molecules between brain immune cells post-TBI.
- To determine how MPs contribute to the systemic circulation and inflammation propagation following brain trauma.
- To explore MPs derived from activated microglia as potential therapeutic targets.
Main Methods:
- Controlled cortical impact TBI was induced in adult male C57BL/6 mice.
- Enriched MPs were isolated from blood and characterized by flow cytometry.
- Pro-inflammatory mediators within MPs were quantified using gene and protein markers.
- Immune propagation assays involved co-culturing MPs with microglial cells.
- MPs from activated microglia were stereotactically injected into the cortex of uninjured mice to assess in vivo neuroinflammation seeding.
Main Results:
- Microglial-derived MPs are released into circulation during the developing neuroinflammatory response post-TBI.
- Circulating MPs from TBI animals can activate microglia in vitro.
- Lipopolysaccharide stimulation enhanced MP release and pro-inflammatory content (IL-1β, miR-155) from microglia.
- MPs isolated from activated microglia were sufficient to initiate neuroinflammation upon injection into naive mouse cortex.
Conclusions:
- Microparticles loaded with pro-inflammatory molecules mediate the development and dissemination of neuroinflammation after TBI.
- These MPs activate additional microglia, potentially driving progressive neuroinflammation and systemic immune responses.
- MPs derived from activated microglia represent a potential therapeutic target for neurological disorders involving neuroinflammation.
