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A cytochemical study of cerebrovascular lesions in mice infected with Plasmodium berghei
T W Polder1, W M Eling, C R Jerusalem
1Department of Neurosurgery, University Hospital Nijmegen, The Netherlands.
Abstract:
Mice with a Plasmodium berghei infection exhibit morphological and cytochemical changes in the blood-brain barrier. Changes in activity and localization of alkaline phosphatase and adenosine triphosphatase, enzymes with important functions in the maintenance of the blood-brain barrier, were observed. Changes in activity and localization of those enzymes in and near the endothelial cells of the microvasculature, concomitant with an increase in pinocytotic activity, and formation of irregular cytoplasmic extensions in these cells, as well as loosening of the basal lamina are indicative of a functional deterioration of the blood-brain barrier in the course of infection.
Insights
Plasmodium berghei infection in mice alters the blood-brain barrier. Key enzymes show changed activity and location, indicating a breakdown of this crucial protective barrier during infection.
Area of Science:
- Neuroscience
- Parasitology
- Cell Biology
Background:
- The blood-brain barrier (BBB) protects the central nervous system from harmful substances.
- Plasmodium berghei is a parasite that causes malaria, a disease that can affect the brain.
Purpose of the Study:
- To investigate the effects of Plasmodium berghei infection on the morphological and cytochemical properties of the blood-brain barrier in mice.
Main Methods:
- Mice infected with Plasmodium berghei were analyzed for changes in the BBB.
- Enzyme activity and localization of alkaline phosphatase and adenosine triphosphatase were assessed.
- Ultrastructural changes in endothelial cells and the basal lamina were examined.
Main Results:
- Significant alterations in alkaline phosphatase and adenosine triphosphatase activity and localization were observed in BBB endothelial cells.
- Increased pinocytotic activity and irregular cytoplasmic extensions were noted in endothelial cells.
- Evidence of basal lamina loosening was present, suggesting BBB compromise.
Conclusions:
- Plasmodium berghei infection leads to functional deterioration of the blood-brain barrier.
- Enzyme changes and ultrastructural alterations in endothelial cells contribute to BBB dysfunction during infection.