Neuroinflammation, which is a fundamental reaction to brain injury, is characterized by the activation of resident microglia and astrocytes and local expression of a wide range of inflammatory mediators. Acute and chronic neuroinflammation has been studied in the mouse brain following exposure to HZE. The acute effect of HZE is detectable at 6 and 9 Gy; no studies are available at lower doses. Myeloid cell recruitment appears by 6 months following exposure. The estimated RBE value of HZE irradiation for induction of an acute neuroinflammatory response is three compared to that of gamma irradiation. COX-2 pathways are implicated in neuroinflammatory processes that are caused by low-LET radiation. COX-2 up-regulation in irradiated microglia cells leads to prostaglandin E2 production, which appears to be responsible for radiation-induced gliosis (overproliferation of astrocytes in damaged areas of the CNS).
