Dexamethasone inhibits brain apoptosis in mice with eosinophilic meningitis caused by Angiostrongylus cantonensis infection
Autor: | Susan Shin Jung Lee, Chuan-Min Yen, Yao Shen Chen, Shue Ren Wann, Bi Yao Lee, Hung Chin Tsai |
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Jazyk: | angličtina |
Předmět: |
Pathology
medicine.medical_specialty Eosinophilic Meningitis Blotting Western Apoptosis Biology Blood–brain barrier Dexamethasone Mice chemistry.chemical_compound In Situ Nick-End Labeling medicine Corticosteroid Animals Immunologic Factors Meningitis Strongylida Infections Evans Blue Mice Inbred BALB C TUNEL assay Research Angiostrongylus cantonensis Brain medicine.disease biology.organism_classification Immunohistochemistry Disease Models Animal medicine.anatomical_structure Infectious Diseases chemistry Blood brain barrier Parasitology Eosinophilic meningitis Injections Intraperitoneal medicine.drug |
Zdroj: | Parasites & Vectors |
ISSN: | 1756-3305 |
DOI: | 10.1186/s13071-015-0792-7 |
Popis: | 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. |
Databáze: | OpenAIRE |
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