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Dexamethasone downregulated the expression of CSF 14-3-3β protein in mice with eosinophilic meningitis caused by Angiostrongylus cantonensis infection.
Acta Trop. 2014 Mar; 131:98-103.AT

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.

Authors+Show Affiliations

Section of Infectious Diseases, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, and National Yang-Ming University, Taipei, Taiwan, ROC. Electronic address: hctsai1011@yahoo.com.tw.Section of Infectious Diseases, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, and National Yang-Ming University, Taipei, Taiwan, ROC.Department of Parasitology and Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, ROC.Section of Infectious Diseases, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, and National Yang-Ming University, Taipei, Taiwan, ROC.Section of Infectious Diseases, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, and National Yang-Ming University, Taipei, Taiwan, ROC.Section of Infectious Diseases, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, and National Yang-Ming University, Taipei, Taiwan, ROC.Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan, ROC. Electronic address: minghongtai@gmail.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24361722

Citation

Tsai, Hung-Chin, et al. "Dexamethasone Downregulated the Expression of CSF 14-3-3β Protein in Mice With Eosinophilic Meningitis Caused By Angiostrongylus Cantonensis Infection." Acta Tropica, vol. 131, 2014, pp. 98-103.
Tsai HC, Lee BY, Yen CM, et al. Dexamethasone downregulated the expression of CSF 14-3-3β protein in mice with eosinophilic meningitis caused by Angiostrongylus cantonensis infection. Acta Trop. 2014;131:98-103.
Tsai, H. C., Lee, B. Y., Yen, C. M., Wann, S. R., Lee, S. S., Chen, Y. S., & Tai, M. H. (2014). Dexamethasone downregulated the expression of CSF 14-3-3β protein in mice with eosinophilic meningitis caused by Angiostrongylus cantonensis infection. Acta Tropica, 131, 98-103. https://doi.org/10.1016/j.actatropica.2013.12.006
Tsai HC, et al. Dexamethasone Downregulated the Expression of CSF 14-3-3β Protein in Mice With Eosinophilic Meningitis Caused By Angiostrongylus Cantonensis Infection. Acta Trop. 2014;131:98-103. PubMed PMID: 24361722.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dexamethasone downregulated the expression of CSF 14-3-3β protein in mice with eosinophilic meningitis caused by Angiostrongylus cantonensis infection. AU - Tsai,Hung-Chin, AU - Lee,Bi-Yao, AU - Yen,Chuan-Min, AU - Wann,Shue-Ren, AU - Lee,Susan Shin-Jung, AU - Chen,Yao-Shen, AU - Tai,Ming-Hong, Y1 - 2013/12/18/ PY - 2013/06/07/received PY - 2013/10/20/revised PY - 2013/12/09/accepted PY - 2013/12/24/entrez PY - 2013/12/24/pubmed PY - 2014/10/4/medline KW - 14-3-3β protein KW - Angiostrongylus cantonensis KW - Blood brain barrier KW - Corticosteroid KW - Eosinophilic meningitis KW - Mice SP - 98 EP - 103 JF - Acta tropica JO - Acta Trop VL - 131 N2 - 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. SN - 1873-6254 UR - https://www.unboundmedicine.com/medline/citation/24361722/Dexamethasone_downregulated_the_expression_of_CSF_14_3_3β_protein_in_mice_with_eosinophilic_meningitis_caused_by_Angiostrongylus_cantonensis_infection_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0001-706X(13)00358-6 DB - PRIME DP - Unbound Medicine ER -