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Tight Junctional Damage in Experimental Mumps‐Associated Hydrocephalus
Author(s) -
UNO Masaaki,
TAKANO Tomoyuki,
YAMANO Tsunekazu,
SHIMADA Morimi
Publication year - 1997
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/j.1741-4520.1997.tb00974.x
Subject(s) - tight junction , choroid plexus , mumps virus , hydrocephalus , blood–brain barrier , pathology , ependyma , cerebrospinal fluid , medicine , cell junction , septate junctions , anatomy , central nervous system , biology , virus , virology , cell , microbiology and biotechnology , genetics , radiology
Tight junctions in the central nervous system (CNS) are a major component of brain barriers including the blood‐brain barrier (BBB) and blood‐CSF barrier, which regulate solute entry and protect against invasion by microorganisms. In this study, we examined the breach of tight junctions in mumps virus‐induced hydrocephalic brain in hamsters using antibodies to Laminin B1 chain and zonula occludentes (ZO‐1) immuno‐histochemistry, and evaluated the role of tight junctions in the pathogenesis of hydrocephalus after mumps virus infection. In suckling hamsters intracerebrally inoculated with mumps virus, severe periventricular edema, ependymal cell loss, and ventricular dilation were observed. ZO‐1‐immunoreactive tight junctions in the hydrocephalic brains were severely damaged in the choroid plexus and ependyma, and in white matter capillaries as early as 3 days after inoculation. These changes were suspected to increase the permeability in blood‐brain and blood‐CSF barriers, leading to periventricular edema. We concluded that the pathologic features of mumps virus‐induced hydrocephalus are intimately related to the breach of tight junctions.