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Departments of
*
Pathology and
Microbiology/Immunology, Albert Einstein College of Medicine, Bronx, NY 10461;
Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY 10595; and
§
Department of Pediatrics, Wayne State University School of Medicine, Detroit, MI 48201
The migration of leukocytes across the blood-brain barrier (BBB)
into the central nervous system is critical in the pathogenesis of
central nervous system inflammatory diseases. The production of
chemokines, such as monocyte-chemoattractant protein-1 (MCP-1), by
endothelial cells (EC) and astrocytes may initiate and amplify this
process. Using a coculture of human EC and astrocytes to model the BBB,
we demonstrated that exogenous MCP-1 induces the transmigration of
monocytes in a dose-dependent manner. TNF-
, IFN-
, or IL-1ß
treatment of cocultures also induced significant migration of monocytes
that correlates with the induction of MCP-1 protein. TGF-ß,
previously shown to induce MCP-1 expression in astrocytes, but not in
EC, caused migration of monocytes across cocultures, but not across EC
grown alone. Monocytes and lymphocytes transmigrated across
cytokine-treated cocultures in greater numbers than across EC alone.
Astrocytes were the main source of cytokine-induced MCP-1, supporting a
role for astrocytes in facilitating leukocyte transmigration. A
blocking Ab to MCP-1 inhibited MCP-1- and cytokine-induced
transmigration of monocytes by 85–90%. Cytokine treatment of
cocultures also resulted in the transmigration of activated,
CD69-positive lymphocytes. The MCP-1-mediated transmigration of
monocytes across cocultures was blocked using an Ab to ICAM-1 and
inhibited by 55% using an Ab to E-selectin. These data suggest a
central role for astrocyte-derived MCP-1 in directing the migration of
monocytes and lymphocytes across the BBB.
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