Decoy receptor-3 (DcR3) is a member of the TNF receptor superfamily of
proteins, which has been implicated in anti-apoptotic and
anti-inflammatory pathways, via binding to TL1A, LIGHT and Fas-L. The
role of the TL1A/DcR3 ligand/receptor pair in ulcerative colitis (UC)
has not been studied. We investigated the systemic (peripheral blood)
and local (large intestine) expression of DcR3 and TL1A in 64 patients
with UC and 56 healthy controls. DcR3 serum concentrations were highly
elevated in patients with active UC (P < 0.0001 vs. healthy controls).
This elevation was clearly related to the presence of intestinal
inflammation as it was less frequently observed in patients in remission
(P=0.003 vs. active UC) whereas effective treatment resulted in
disappearance or significant decrease of serum DcR3 (P=0.006 vs.
pre-treatment). Furthermore, DcR3 mRNA transcripts were significantly
elevated in inflamed areas of the colon (P=0.002 vs. non-affected of the
same patient). In addition to DcR3 elevation, we found increased
circulating levels of TL1A in patients with either active or inactive UC
in comparison to healthy controls (P < 0.001 for both). We conclude that
elevated serum DcR3 may serve as an indicator of active colonic
inflammation in patients with UC. TL1A/DcR3-mediated pathways may
participate in the pathogenesis of UC. (C) 2010 Elsevier Inc. All rights
reserved
