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Critical role for scavenger receptor CD36 in microparticle-mediated neuroinflammation in a murine model of
Abid R Bhat1, Awadhesh K Arya1, Zuha Imtiyaz1
1Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland, United States.
Abstract:
Blood-borne microparticles (MPs) play a role in several forms of brain injury, but how they interact with the vasculature and contribute to neuroinflammation is unknown. The scavenger receptor CD36 is expressed across various cell types and regulates inflammation, vascular function, and innate immunity. We hypothesized that CD36 mediates MPs-induced neuroinflammatory responses in a murine model of decompression sickness (DCS). Wild-type mice subjected to decompression and naïve mice injected with MPs from decompressed mice exhibited a 2.2 ± 0.5-fold elevation in perivascular MPs deposition, 2.8 ± 0.6-fold elevation of inflammatory MPs in blood and 2.4 ± 0.4-fold in cervical lymph nodes, 2.7 ± 0.6-fold increase in neutrophil activation, 2.0 ± 0.3-fold increased glymphatic flow, 3.1 ± 0.4-fold increased leakage of six megadalton dextran at the blood-brain barrier, and a doubling of inflammatory proteins in brain. These events failed to occur in CD36 knockout mice and those conditionally deficient in endothelial CD36 (FLOX). We conclude that inflammatory MPs interact with endothelial CD36 to mediate neuroinflammatory responses and vascular injury in DCS.NEW & NOTEWORTHY Elevated glymphatic flow, glial cell activation, increased circulating microparticles (MPs), and neutrophil activation due to decompression have been well documented in animal models. This report shows that filamentous (F)-actin expressing MPs produced postdecompression interact with endothelial CD36 driving a feed-forward neuroinflammatory cycle and inducing vascular injury.
Insights
Blood-borne microparticles trigger neuroinflammation and brain injury in decompression sickness. The scavenger receptor CD36 mediates these effects by interacting with microparticles, leading to vascular damage.
Area of Science:
- Neuroscience
- Immunology
- Vascular Biology
Background:
- Blood-borne microparticles (MPs) are implicated in brain injury.
- The scavenger receptor CD36 regulates inflammation and vascular function.
- The role of MPs in decompression sickness (DCS)-induced neuroinflammation is unclear.
Purpose of the Study:
- To investigate the role of CD36 in mediating MPs-induced neuroinflammation in a murine model of DCS.
- To determine if CD36 facilitates MPs interaction with the vasculature and contributes to neuroinflammation.
Main Methods:
- Utilized a murine model of decompression sickness (DCS).
- Compared wild-type mice with CD36 knockout and endothelial CD36-deficient mice.
- Administered microparticles (MPs) from decompressed mice to wild-type mice.
- Assessed perivascular MPs deposition, inflammatory MPs, neutrophil activation, glymphatic flow, blood-brain barrier permeability, and brain inflammatory protein levels.
Main Results:
- Decompression induced significant increases in perivascular MPs, circulating inflammatory MPs, neutrophil activation, glymphatic flow, blood-brain barrier leakage, and brain inflammatory proteins.
- These DCS-induced effects were abolished in CD36 knockout and endothelial CD36-deficient mice.
- MPs from decompressed mice increased perivascular deposition and inflammatory markers in wild-type mice.
Conclusions:
- Endothelial CD36 mediates MPs-induced neuroinflammatory responses and vascular injury in DCS.
- MPs interact with endothelial CD36 to promote a feed-forward neuroinflammatory cycle.
- Targeting CD36 may offer a therapeutic strategy for DCS-related brain injury.
