Treatment with MβCD, which prevents caveola formation, resulted in a Cav-1-induced decrease in meningoencephalitis in A. cantonensis infection, leading to a decrease in MMP-9 activity in the brain and CSF, as well as degradation of tight junction proteins (Zo-1 and claudin-5), thus mitigating damage to the BBB. The gene discussed is CLDN5; the disease is meningoencephalitis.