دورية أكاديمية
Erythropoietin treatment alleviates ultrastructural myelin changes induced by murine cerebral malaria
العنوان: | Erythropoietin treatment alleviates ultrastructural myelin changes induced by murine cerebral malaria |
---|---|
المؤلفون: | Hempel Casper, Hyttel Poul, Staalsø Trine, Nyengaard Jens R, Kurtzhals Jørgen AL |
المصدر: | Malaria Journal, Vol 11, Iss 1, p 216 (2012) |
بيانات النشر: | BMC, 2012. |
سنة النشر: | 2012 |
المجموعة: | LCC:Arctic medicine. Tropical medicine LCC:Infectious and parasitic diseases |
مصطلحات موضوعية: | Cerebral malaria, Plasmodium berghei ANKA, Demyelination, Neurological sequelae, Erythropoietin, Arctic medicine. Tropical medicine, RC955-962, Infectious and parasitic diseases, RC109-216 |
الوصف: | Abstract Background Cerebral malaria (CM) is a severe complication of malaria with considerable mortality. In addition to acute encephalopathy, survivors frequently suffer from neurological sequelae. The pathogenesis is incompletely understood, hampering the development of an effective, adjunctive therapy, which is not available at present. Previously, erythropoietin (EPO) was reported to significantly improve the survival and outcome in a murine CM model. The study objectives were to assess myelin thickness and ultrastructural morphology in the corpus callosum in murine CM and to adress the effects of EPO treatment in this context. Methods The study consisted of two groups of Plasmodium berghei-infected mice and two groups of uninfected controls that were either treated with EPO or placebo (n = 4 mice/group). In the terminal phase of murine CM the brains were removed and processed for electron microscopy. Myelin sheaths in the corpus callosum were analysed with transmission electron microscopy and stereology. Results The infection caused clinical CM, which was counteracted by EPO. The total number of myelinated axons was identical in the four groups and mice with CM did not have reduced mean thickness of the myelin sheaths. Instead, CM mice had significantly increased numbers of abnormal myelin sheaths, whereas EPO-treated mice were indistinguishable from uninfected mice. Furthermore, mice with CM had frequent and severe axonal injury, pseudopodic endothelial cells, perivascular oedemas and intracerebral haemorrhages. Conclusions EPO treatment reduced clinical signs of CM and reduced cerebral pathology. Murine CM does not reduce the general thickness of myelin sheaths in the corpus callosum. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1475-2875 |
Relation: | http://www.malariajournal.com/content/11/1/216; https://doaj.org/toc/1475-2875 |
DOI: | 10.1186/1475-2875-11-216 |
URL الوصول: | https://doaj.org/article/8a7f799b1e124652b7e5035aa4f084a9 |
رقم الأكسشن: | edsdoj.8a7f799b1e124652b7e5035aa4f084a9 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 14752875 |
---|---|
DOI: | 10.1186/1475-2875-11-216 |