Dexamethasone inhibits brain apoptosis in mice with eosinophilic meningitis caused by Angiostrongylus cantonensis infection

Particle and Fibre Toxicology

Yao-Shen Chen²  Susan Shin-Jung Lee²  Shue-Ren Wann²  Chuan-Min Yen³  Bi-Yao Lee²  Hung-Chin Tsai¹ 

[1] National Defense Medical Center, Taipei, Taiwan;Section of Infectious Diseases, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan and National Yang-Ming University, Taipei, Taiwan;Department of Parasitology and Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan

关键词: Eosinophilic meningitis;    Corticosteroid;    Blood brain barrier;    Apoptosis;    Angiostrongylus cantonensis;   

Others  :  1145975
DOI  :  10.1186/s13071-015-0792-7

 received in 2014-10-31, accepted in 2015-03-10,  发布年份 2015

【 摘 要 】

Background

Angiostrongylus cantonensis, the rat lungworm, is the major cause of eosinophilic meningitis worldwide. Rats serve as the definitive host of the nematode, but humans can be infected incidentally, leading to eosinophilic meningitis. A previous BALB/c animal study has demonstrated increased apoptotic proteins and decreased anti-apoptotic proteins in mice infected with A. cantonensis. Steroids may be an effective treatment option for eosinophilic meningitis caused by A. cantonensis, but the involved mechanism is unclear. This study hypothesized that the beneficial effects of steroids on eosinophilic meningitis are mediated by decreased apoptosis.

Methods

In a BALB/c animal model, mice were orally infected with 50 A. cantonensis L3 via an oro-gastric tube and were sacrificed every week for 3 consecutive weeks after infection or until the end of the study. Dexamethasone was injected intra-peritoneally from the 7^th day post-infection until the end of the 21-day study. Evans blue method was used to measure changes in the blood brain barrier, while western blotting, immuno-histochemistry, and TUNEL assay were used to analyze brain homogenates expression of apoptotic and anti-apoptotic proteins.

Results

There were increased amounts of Evans blue, apoptotic proteins (caspase-3, -8, and -9 and cytochrome C), and decreased anti-apoptotic proteins (bcl-2) after 2-3 weeks of infection. Dexamethasone administration significantly decreased Evans blue extravasations and apoptotic protein expressions.

Conclusions

Apoptosis of mice brain homogenates can be repressed by dexamethasone treatment.

【 授权许可】

   
2015 Tsai et al.; licensee BioMed Central.

【 图 表 】

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