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MediCity Research Laboratory, Turku University, and National Public Health Institute, Turku, Finland
Reactive arthritis can be triggered by inflammatory bowel diseases.
We hypothesized that migration of mucosal immune cells from inflamed
gut to joints could contribute to the development of reactive
arthritis. Here we isolated gut-derived leukocytes from patients with
Crohn’s disease and ulcerative colitis. Using function-blocking mAbs
and in vitro frozen section adhesion assays we studied whether these
cells bind to synovial vessels and which molecules mediate the
interaction. The results showed that mucosal leukocytes from
inflammatory bowel diseased gut bind well to venules in synovial
membrane. Small intestinal lymphocytes adhered to synovial vessels
using multiple homing receptors and their corresponding endothelial
ligands (CD18-ICAM-1,
4
7/41-integrin-VCAM-1,
L-selectin-peripheral lymph node addressins, and CD44). Of these, only
ICAM-1 significantly supported binding of immunoblasts. In contrast,
P-selectin glycoprotein ligand-1-P-selectin interaction accounted for
practically all synovial adherence of mucosal macrophages. In addition,
blocking of vascular adhesion protein-1 significantly inhibited binding
of all these leukocyte subsets to joint vessels. We conclude that
different leukocyte populations derived from inflamed gut bind avidly
to synovial vessels using distinct repertoire of adhesion molecules,
suggesting that their recirculation may contribute to the development
of reactive arthritis in inflammatory bowel
diseases.
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