Soluble Fas/FasLare elevated in the serum and cerebrospinal fluid of patients with neurocysticercosis.

Neurocysticercosis (NCC) caused by Taeniasolium is one of the most common parasitic diseases of the central nervous system. Inflammation and apoptosis are two main responses involved in NCC pathogenesis. We aimed to examine apoptosis by the TUNEL assay and apoptosis-associated sFas and sFasL levels in the cerebrospinal fluid (CSF) and serum of patients with NCC. Brain biopsy (n = 1), CSF (n = 14), and serum (n = 36) of patients with NCC and uninfected controls (n = 14 and 24 for CSF and serum, respectively) were collected together with clinical data. Residual brain tissue was analyzed by the TUNEL assay. sFas and sFasL in CSF samples and sFas, sFasL, and p53 in serum samples were measured by ELISA. Immunohistochemistry of the biopsy indicated the presence of vimentin-positive arachnoid tissue in the TUNEL-positive region. Compared to controls, sFas was significantly reduced in CSF samples of patients with NCC (P = 0.018), especially among those without inflammation, but significantly increased in the serum samples of the vesicular(P = 0.011), moderate(P = 0.025), and non-epilepsy(P = 0.049) subgroups of patients with NCC. sFasL was elevated in the CSF (P < 0.0001), as well as in the calcified subgroup (P = 0.031), but sFasL levels in CSF were similar among patients with NCC with and without inflammation. These findings support a role of sFas and sFasL in the induction of apoptosis in patients with NCC, with sFas probably being involved in the inflammation phase of NCC and depending on host factors such as parasite stage, disease severity, and symptoms, and sFasL being involved in the inflammation, non-inflammation, and calcification phase of the disease.