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Department of Pediatrics, Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada
Monocytes migrate through vascular endothelium, and then in
connective tissue. As a model of this process, we investigated adhesion
molecules involved in monocyte migration through HUVEC and a barrier of
human synovial fibroblasts (HSF). Minimal spontaneous monocyte
migration (6–7%) occurred through either cell barrier, but this
increased markedly (27–35% of added monocytes) when a C5a chemotactic
gradient was present. Migration across unstimulated HUVEC was partially
inhibited (40%) by mAb to CD18 (ß2 integrin) and
completely blocked by anti-CD18 plus anti-
4
(CD49d; very late Ag-4 (VLA-4)) mAbs. In contrast, migration across HSF
induced by C5a or monocyte chemoattractant protein-1 was not inhibited
by mAb to CD18 and was only partially inhibited (33%) in combination
with anti-4 mAb. The CD18- and VLA-4-independent
migration across HSF was completely inhibited by mAb to
5 of VLA-5. The inhibitory effect of mAbs to VLA-4 and
VLA-5 was on the monocyte and required blockade of CD11/CD18 to be
observed. In contrast to HSF, no role for VLA-5 in monocyte
transendothelial migration was detected. Both HSF and IL-1-stimulated
HUVEC expressed vascular cell adhesion molecule-1 (VCAM-1). However,
VLA-4-mediated monocyte migration across HSF was only partially
dependent on VCAM-1, in contrast to transendothelial migration, which
was completely blocked by anti-VCAM-1 mAbs. In conclusion, unlike
transendothelial migration, for which VLA-4 is the alternative
mechanism to CD11/CD18 on monocytes, both VLA-4 and VLA-5 can mediate
monocyte migration through fibroblast barriers. In addition to VCAM-1,
other ligand(s) on HSF are also involved in the VLA-4-mediated
migration.
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