A significant complication of angiostrongyliasis remains eosinophilic meningoencephalitis, leading to patients' neurological deterioration, cerebral palsy, and respiratory changes, resulting in death. Clinically, A. cantonensis-infected patients sometimes showed decreased CSF glucose levels. Animal models infected with A. cantonensis have also reported a reduced serum glucose profile. While the brain uses glucose as the primary fuel source, glycolysis is essential for various neural activities in the brain. The defection of the glycolytic pathway has also been found to closely correlate to neurodegenerative diseases such as Alzheimer's disease. However, the role of glycolysis in the pathology and neurological declines associated with A. cantonensis infection remains unknown. Our current study has shown that A. cantonensis infection increases glucose content in the brain and suppresses the expression of the glycolytic enzymes in the brain. Glycolytic products such as pyruvate and ATP were also decreased in their level in the brain. This suppression of brain glycolysis was found to be correlated to the host's histopathology and neurological symptoms. Further analysis using mice infected with a different number of third-stage larvae (L3) A. cantonensis revealed that the defection of glycolysis was indeed caused by the presence of fifth-stage larvae (L5) of A. cantonensis in the brain of experimental mice. However, it may not be directly related to the damage that L5 caused to the brain. Our study delineates some aspects of the pathophysiology of angiostrongyliasis and may provide potential therapeutic targets for the future.
Keywords: Angiostrongyliasis; Angiostrongylus cantonensis; Glycolysis; Meningoencephalitis.
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