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

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• 作者：Hung-Chin Tsai (1) (3)
  Bi-Yao Lee (1)
  Chuan-Min Yen (2)
  Shue-Ren Wann (1)
  Susan Shin-Jung Lee (1)
  Yao-Shen Chen (1)
  
  1. Section of Infectious Diseases ; Department of Medicine ; Kaohsiung Veterans General Hospital ; Kaohsiung ; Taiwan and National Yang-Ming University ; Taipei ; Taiwan
  3. National Defense Medical Center ; Taipei ; Taiwan
  2. Department of Parasitology and Graduate Institute of Medicine ; Kaohsiung Medical University ; Kaohsiung ; Taiwan
  
• 关键词：Angiostrongylus cantonensis ; Apoptosis ; Blood brain barrier ; Corticosteroid ; Eosinophilic meningitis
• 刊名：Parasites & Vectors
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：8
• 期：1
• 全文大小：1,871 KB
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• 刊物主题：Parasitology; Infectious Diseases; Tropical Medicine; Entomology;
• 出版者：BioMed Central
• ISSN：1756-3305

文摘

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 7th 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.