AIMS/HYPOTHESIS: High levels of @entity32 locally in the graft during the initial days after transplantation can cause primary non-function (PNF) of grafted xenogeneic islets in @entity9719 @entity19 . The aim of this study was to explore in a model of spontaneous @entity6 , the @entity9719 @entity19 , the potential of anti-inflammatory agents in the prevention of PNF after xenogeneic islet transplantation. METHODS: Spontaneously @entity6 @entity9719 @entity19 were transplanted with 300 @entity35 islets. Animals were treated with @entity117 ( @entity1281 ), @entity13586 , TGF-beta or @entity18995 ( @entity18995 ). Intra-graft expression of @entity32 -related molecules was measured by real time PCR 8 h post-transplantation. At the same time point, plasma @entity3542 levels were measured. RESULTS: Xenogeneic islets transplanted in control spontaneously @entity6 @entity19 resulted in PNF in 16 out of 38 @entity19 (42%). Initial graft loss was not altered by administration of @entity13586 (30%) or TGF-beta (25%). @entity1281 reduced the rate of rapid graft loss to 8% ( p<0.05 vs controls) and administration of @entity18995 even totally prevented PNF (0%, p<0.05 vs controls). Furthermore, all therapies prolonged the mean survival time of xenogeneic islet grafts. The inhibition of PNF by @entity1281 was associated with decreased intra-islet levels of @entity32 -related molecules (IL-1, @entity637 , @entity13633 , @entity10178 ) and chemokines ( @entity8929 and @entity13948 ). Finally, also a diminished production of systemic @entity3542 levels was observed in @entity1281 - and @entity18995 -treated islet recipients. CONCLUSIONS/INTERPRETATION: These data show that treatment with @entity1281 or @entity18995 prevents PNF after islet transplantation in spontaneously @entity6 @entity9719 @entity19 . Moreover, the involvement of non-specific @entity32 is recognized in xenogeneic islet PNF in spontaneously @entity6 @entity9719 @entity19 .

Prevention of primary non-function of islet xenografts in autoimmune @entity6 XXXX mice by anti-inflammatory agents.

@entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity13586 :: ('MESH:C116926', 'Chemical') :: ['rofecoxib'] @entity10178 :: ('17709(Tax:10090)', 'Gene') :: ['COX-2'] @entity9719 :: ('MESH:D020191', 'Disease') :: ['NOD'] @entity8929 :: ('17224(Tax:10090)', 'Gene') :: ['MCP-1'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetic', 'diabetes'] @entity19 :: ('10090', 'Species') :: ['mice', 'mouse'] @entity117 :: ('MESH:D001241', 'Chemical') :: ['acetylsalicylic acid'] @entity3542 :: ('CHEBI:16301', 'Chemical') :: ['nitrite'] @entity13633 :: ('18126(Tax:10090)', 'Gene') :: ['iNOS'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity13948 :: ('20297(Tax:10090)', 'Gene') :: ['MIP-3alpha'] @entity1281 :: ('CHEBI:15365', 'Chemical') :: ['AsA'] @entity637 :: ('21926(Tax:10090)', 'Gene') :: ['TNF-alpha'] @entity18995 :: ('16181(Tax:10090)', 'Gene') :: ['IL-1ra', 'IL-1 receptor antagonist']
@entity9719 :: (MESH:D020191,Disease) :: ['NOD']
