| Literature DB >> 24361722 |
Hung-Chin Tsai1, Bi-Yao Lee2, Chuan-Min Yen3, Shue-Ren Wann2, Susan Shin-Jung Lee2, Yao-Shen Chen2, Ming-Hong Tai4.
Abstract
Angiostrongylus cantonensis is the main causative agent of human eosinophilic meningitis in Southeast Asia and the Pacific Islands. A previous study demonstrated that the 14-3-3β protein is a neuropathological marker in monitoring neuronal damage in meningitis. Steroids are commonly used in patients with eosinophilic meningitis caused by A. cantonensis infection. However, the mechanism by which steroids act in eosinophilic meningitis is unknown. We hypothesized that the beneficial effect of steroids on eosinophilic meningitis is partially mediated by the down-regulation of 14-3-3β protein expression in the cerebrospinal fluid (CSF). In this animal study, we determined the dynamic changes of 14-3-3β protein in mice with eosinophilic meningitis. The 14-3-3β protein in serum and CSF was increased in week 2 and 3 after infections. Dexamethasone administration significantly decreased the amounts of CSF 14-3-3β protein. By developing an in-house ELISA to measure 14-3-3β protein, it was found that the amounts of 14-3-3β protein in the CSF and serum increased over a three-week period after infection. There was a remarkable reduction of 14-3-3β protein in the CSF after 2 weeks of dexamethasone treatment. In conclusion, the administration of corticosteroids in mice with eosinophilic meningitis decreased the expression of 14-3-3β protein in the CSF.Entities:
Keywords: 14-3-3β protein; Angiostrongylus cantonensis; Blood brain barrier; Corticosteroid; Eosinophilic meningitis; Mice
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Year: 2013 PMID: 24361722 DOI: 10.1016/j.actatropica.2013.12.006
Source DB: PubMed Journal: Acta Trop ISSN: 0001-706X Impact factor: 3.112