Recombinant human plasma gelsolin suppresses persistent neuroinflammation and restores hippocampal neurogenesis in murine model of decompression sickness

A decrease in plasma gelsolin levels and the release of inflammatory microparticles (MPs) occur in response to high pressure followed by decompression, with expression of filamentous (F)-actin leading to persistent neuroinflammation and functional deficits lasting at least 12 days. The infusion of recombinant human plasma gelsolin lyses these MPs in decompressed mice, thereby alleviating particle-associated neuronal dysfunction. Rhu-gelsolin infusion may be beneficial as a prophylactic or treatment for decompression sickness.