Blood-brain barrier impairment with enhanced SP, NK-1R, GFAP and Claudin-5 expressions in experimental cerebral toxocariasis

Infection by Toxocara canis in humans may cause cerebral toxocariasis (CT). Appreciable numbers of T. canis larvae cross the blood-brain barrier (BBB) to invade the brain thus causing CT. In the present studies, we evaluated the BBB permeability and BBB injury as assessed by the cerebral Evans blue...

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Bibliographic Details
Published in:Parasite immunology 2008-10, Vol.30 (10), p.525-534
Main Authors: LIAO, C.-W, CHO, W.-L, KAO, T.-C, SU, K.-E, LIN, Y.-H, FAN, C.-K
Format: Article
Language:English
Subjects:
Animals
blood-brain barrier
Blood-Brain Barrier - parasitology
Blood-Brain Barrier - physiopathology
Brain - parasitology
Brain - pathology
cerebral toxocariasis
Claudin-5
Evans Blue
Female
Gene Expression
glial fibrillary acidic protein
Glial Fibrillary Acidic Protein - metabolism
Membrane Proteins - metabolism
Mice
Mice, Inbred ICR
NK-1 receptor
Receptors, Neurokinin-1 - metabolism
RNA, Messenger - metabolism
substance P
Substance P - metabolism
Time Factors
Toxocara
Toxocara canis
Toxocariasis - genetics
Toxocariasis - pathology
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Summary:Infection by Toxocara canis in humans may cause cerebral toxocariasis (CT). Appreciable numbers of T. canis larvae cross the blood-brain barrier (BBB) to invade the brain thus causing CT. In the present studies, we evaluated the BBB permeability and BBB injury as assessed by the cerebral Evans blue (EB) concentration as well as by pathological changes and glial fibrillary acidic protein (GFAP) expression in T. canis-infected mice monitored from 3 days (dpi) to 8 weeks post-infection (wpi). The vasodilation neuropeptides, the expressions of substance P (SP) and its preferred binding neurokinin-1 receptor (NK-1R) as well as claudin-5 of tight-junction proteins associated with BBB impairment were also assessed by Western blotting and reverse-transcriptase polymerase chain reaction. Results revealed that BBB permeability increased as evidenced by a significantly elevated EB concentration in brains of infected mice. BBB injury appeared due to enhanced GFAP protein and mRNA expressions from 4 to 8 wpi. Leukocytes might have been unrelated to BBB impairment because there was no inflammatory cell infiltration despite T. canis larvae having invaded the brain; whereas markedly elevated SP protein and NK-1R mRNA expressions concomitant with enhanced claudin-5 expression seemed to be associated with persistent BBB impairment in this experimental CT model.
ISSN:0141-9838
1365-3024
DOI:10.1111/j.1365-3024.2008.01048.x