Eosinophils support Th2 response and control parasite number in brain during murine neurocysticercosis (MPF7P.717)

Neurocysticercosis (NCC) is a common parasitic infection of the brain and leading cause of acquired epilepsy worldwide. NCC is caused by metacestode larvae of the tapeworm Taenia solium and characterized by an initial asymptomatic phase followed by a symptomatic phase. While the asymptomatic phase is attributed to the immunosuppressive capabilities of viable T. solium metacestodes, dying parasites induce inflammation including an eosinophil (EO) response causing pathology and symptoms. Previous studies in T. solium -infected pigs have shown that EOs are present around dying parasites. However, the role of EOs in killing of metacestode has not been verified. To determine the parasiticidal role of EOs in brain , we used a murine model of NCC in which wild type (WT) or EO deficient (ΔdblGATA) mice were infected intracranially . We found a strong EO response in WT NCC mice similar to porcine NCC. In comparison to WT NCC mice, EO deficient, ΔdblGATA NCC mice had an increased parasite burden. Analysis of infiltrates from infected brains revealed that ΔdblGATA mice had reduced leukocyte infiltration into the brain in comparison to WT mice. However, αβ T cell frequency was greater in ΔdblGATA mice brain. Further, higher αβ T cell frequency correlated with increased CD8 + T cell response and reduced CD4 + Th2 responses. Thus, our results show that EOs support Th2 response in brain microenvironment and play a critical role in controlling the parasite number in brain during murine NCC.