Inflammation of the choroid plexus and ependymal layer of the ventricle following intraventricular hemorrhage.

Intraventricular hemorrhage (IVH), which afflicts thousands of people of all ages every year, frequently results in the development of communicating hydrocephalus. Classically, IVH-induced hydrocephalus has been attributed to reduced resorption of cerebrospinal fluid (CSF) due to dysfunction of arachnoid granulations, but this explanation may be incomplete. We hypothesized that IVH would cause inflammation of the choroid plexus and of the ependymal lining of the ventricles, resulting in dysfunction of these barrier cells. Barrier dysfunction, in turn, would be expected to cause an increase in production of abnormal protein-rich CSF and transependymal migration of CSF. We tested this hypothesis using a rat model of IVH, in which 160 μl of autologous blood was infused into the lateral ventricle, resulting in a twofold increase in ventricular size 48 h later. In this model, we found significant activation of nuclear factor κB (NF-κB) signaling by the CSF barrier cells of the choroid plexus and ependymal lining. Moreover, these inflammatory changes were associated with abnormal uptake of serum-derived IgG by the barrier cells, a phenomenon closely linked to abnormal permeability of the blood-brain barrier. We conclude that inflammation marked by NF-κB signaling is a prominent feature after IVH and may account for certain pathophysiological sequelae associated with IVH.