Upregulation of MMP-9/TIMP-1 enzymatic system in eosinophilic meningitis caused by Angiostrongylus cantonensis
| Autor: | Shih Chan Lai, Jer Yuh Liu, Hsiu Hsiung Lee, Ke Min Chen, Bo Cyuan Tsai, Hui Lin Chou |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Eosinophilic Meningitis
biology Cell Biology Eosinophil medicine.disease biology.organism_classification Molecular biology Pathology and Forensic Medicine Angiostrongylus cantonensis medicine.anatomical_structure Eosinophilic Immunology Angiostrongyliasis medicine Eosinophilia medicine.symptom Molecular Biology Meningitis CSF albumin |
| Zdroj: | International Journal of Experimental Pathology. 86:81-89 |
| ISSN: | 0959-9673 |
| DOI: | 10.1111/j.0959-9673.2005.00413.x |
| Popis: | Proteolysis depends on the balance between the proteases and their inhibitors. Matrix metalloproteinase-9 (MMP-9) and its specific inhibitors, tissue inhibitors of metalloproteinases (TIMP), contribute to eosinophilic inflammatory reaction in the subarachnoid space of the Angiostrongylus cantonensis-infected mice. The expression of MMP-9 in cerebrospinal fluid (CSF) was significantly increased in mice with eosinophilic meningitis, compared to that in uninfected ones. However, the TIMP-1 levels were unchanged and remained at basal levels at all time points, even in uninfected mice. Elevated MMP-9 mRNA expression coincided with protein levels and proteolytic activity, as demonstrated by means of positive immunoreactivity and gelatin zymography. CSF protein contents correlated significantly with MMP-9 intensity and CSF eosinophilia. In addition, immunohistochemistry demonstrated MMP-9 and TIMP-1 localization in eosinophils and macrophages. When the specific MMP inhibitor, GM6001, was added, MMP-9 enzyme activity was reduced by 45.4%. The percentage of eosinophil increased significantly upon the establishment of infection, but subsided upon inhibition. These results show that MMP-9/TIMP-1 imbalance in angiostrongyliasis may be associated with eosinophilic meningitis. |
| Databáze: | OpenAIRE |
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