Scavenger Receptor CD36 regulates neuroinflammatory responses in a murine model of decompression sickness

The scavenger receptor CD36, expressed across various cell types regulates inflammation, vascular function, and innate immunity. We hypothesized that CD36 mediates microparticle (MPs) induced neuroinflammatory response in a murine model of decompression sickness (DCS). Whereas wild type mice exhibited elevations of inflammatory MPs in blood (362 ± 321%) and cervical lymph nodes (251±179 %), neutrophil activation, (137 +/- 41%) elevation of glymphatic flow assessed by fluorescent dye tracer, (332±56%) increase in blood brain barrier leakage assessed by 2 x 10 6 Da dextran uptake and (2.6±0.4) increase in neuroinflammation assess as phosphorylated NF-kB, mice conditionally deficient in endothelial CD36 (offspring from Tie2-Cre X flox CD36 transgenic mice) failed to exhibit these changes. Similar results were also observed with standard CD36 knock-out mice. We conclude that endothelial CD36 is required for inflammatory microparticle communication at the endothelium to mediate neuroinflammatory responses and vascular injury in DCS. This work was supported in part by the US Office of Naval Research under grant No. N0001422-1-2818 and the National Institutes for Health (NINDS) R01-NS122855 (to S. R. Thom). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.