Angiostrongylus cantonensisinfection induces MMP-9 and causes tight junction protein disruption associated with Purkinje cell degeneration

Angiostrongylus cantonensiscauses a human central nervous system (CNS) infection characterized by eosinophilic meningitis or meningoencephalitis. Individuals infected withA. cantonensisexhibit unbalanced walking. The mechanism of extensive neurological impairments of hosts caused byA. cantonensislarvae remains unclear. Tight junction proteins (e.g., claudin-5 and zonula occludens-1) are the most important regulators of paracellular permeability and cellular adhesion. In a previous study, we found that increased matrix metalloproteinase-9 (MMP-9) activity may be associated with blood-CNS barrier disruption and/or the degeneration of Purkinje cells in eosinophilic meningitis caused byA. cantonensis. In the present study, the co-localization of MMP-9 and tight junction proteins on the degeneration of Purkinje cells was measured via confocal laser scanning immunofluorescence microscopy. The statistical evidence indicated that MMP-9 correlated between tight junction protein disruption and Purkinje cell degeneration at 20 days post-infection withA. cantonensis. In conclusion, Purkinje cell degeneration is highly correlated with tight junction protein disruption via the MMP-9 activation pathway.