CONICET | Buscador de Institutos y Recursos Humanos

Spleen-brain inflammatory coupling in a model ofTemporal Lobe Epilepsy Sarchi, P.V; Rossi, A.R;Ramos, A. J. A highpercentage of patients with temporal lobe epilepsy (TLE), one of the mostfrequent neurological diseases, refer an initial precipitating event, such ascomplex febrile seizures during childhood, followed by a silent latency period(LP), until the onset of the chronic seizures phase. Using thelithium-pilocarpine rat model of TLE we have previously shown that neurodegeneration,reactive gliosis and macrophages brain infiltration occur during the LP andthat early interventions limiting immune activation during the LP increaseepileptic threshold during the chronic phase (Rossi et al., 2013; 2017). Wehere studied the peripheral immune cells participation in the LP that followspilocarpine-induced SE. Male Wistar rats were treated with lithium-pilocarpine(127 mg/kg /30 mg/kg) developing SE, that were limited to 20 min by 20 mg/kg i.p.diazepam. Histological analysis of spleen sections 8 h or 1, 2, 3 days post SE(DPSE) showed a peak in the disorganization of the spleen white pulp at 1 DPSE.This disorganization seemed to be spleen-specific since we did not findsignificant changes in the gut-associated lymphoid tissue (GALT). On the otherhand, we found increased abundance of CD4+ lymphocytes in the choroid plexus at3DPSE, suggesting a brain-spleen inflammatory coupling. Accordingly, our lossof function studies performed on splenectomized and sham-operated rats (1wbefore lithium-pilocarpine-induced SE) showed that splenectomy decreasedastrogliosis and neuroinflammation at 7DPSE. Our results suggest thatperipheral immune system is probably responding to specific brain-derived cluestriggered by the SE and the spleen is directly involved in the modulation ofneuroinflammation that follows SE. Supported by PICT 2017-2203; UBACYT; andFONCYT fellowship (PS).