Persistent neuroinflammation and functional deficits in a murine model of decompression sickness.

We hypothesized that early intra-CNS responses in a murine model of decompression sickness (DCS) would be reflected by changes in the microparticles (MPs) that exit the brain via the glymphatic system, and due to systemic responses the MPs would cause inflammatory changes lasting for many days leading to functional neurological deficits. Elevations on the order of 3-fold of blood-borne inflammatory MPs, neutrophil activation, glymphatic flow and neuroinflammation in cerebral cortex and hippocampus were found in mice at 12 days after exposure to 760 kPa of air for 2 hours. Mice also exhibited a significant decline in memory and locomotor activity, as assessed by novel object recognition and rotarod testing. Similar inflammatory changes in blood, neuroinflammation and functional impairments were initiated in naïve mice by injection of filamentous (F-) actin-positiveMPs, but not F-actin-negative MPs,obtained from decompressed mice. We conclude that high pressure/decompression stress establishes a systemic inflammatory process that results in prolonged neuroinflammation and functional impairments in the mouse decompression model.