Exploration of the Molecular Mechanism by Which Caveolin-1 Regulates Changes in Blood–Brain Barrier Permeability Leading to Eosinophilic Meningoencephalitis

Author:

Chen An-Chih1,Lai Shih-Chan23,Lu Cheng-You4ORCID,Chen Ke-Min23ORCID

Affiliation:

1. Department of Neurology, Chung Shan Medical University Hospital, Taichung 40201, Taiwan

2. Department of Parasitology, Chung Shan Medical University, Taichung 40201, Taiwan

3. Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 40201, Taiwan

4. Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung 40227, Taiwan

Abstract

Angiostrongylus cantonensis, a zoonotic parasite, can invade the human central nervous system (CNS) and cause acute eosinophilic meningitis or eosinophilic meningoencephalitis. Mice infected with A. cantonensis show elevated levels of pro-inflammatory cytokines, plasminogen activators, and matrix metalloproteinase-9, resulting in disruption of the blood–brain barrier (BBB) and immune cell infiltration into the CNS. Caveolin-1 (Cav-1) regulates the permeability of the BBB, which affects immune cells and cerebrospinal fluid. This intricate interaction ultimately fuels the progression of brain damage and edema. This study aims to investigate the regulatory role of Cav-1 in the pathogenesis of meningoencephalitis induced by A. cantonensis infection. We investigated pathological alterations by triphenyl-tetrazolium chloride, brain water content, BBB permeability, Western blot analysis, and gelatin zymography in BALB/c mice after A. cantonensis. The study evaluates the critical role of Cav-1 regulation through the TLR4/MyD88 signaling pathway, modulates tight junction proteins, influences BBB permeability, and contributes to brain damage in A. cantonensis-induced meningoencephalitis.

Publisher

MDPI AG

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