S132 Poster Presentations days, starting 5 days before colitis induction until 3th day thereafter. On day 10 of experiment, rats were euthanized and autopsied. The colon was isolated and 10 cm segment of the distal portion was resected and weighed. The isolated distal colon was longitudinally opened and the Mucosal Damage Area (MDA) and the Macroscopic Damage Score (MDS) measured. Cytokines production (IFNg, IL-2, IL10, TNFa) was evaluated in splenocytes from untreated rats isolated and incubated in medium containing ConA (4 mg/ml) and Rifamycin SV in a concentration of 10 9 M and 10 3 M. Detections were performed by ELISA kits. Results: In DNB-induced colitis, rats treated with the irritant alone showed body weight decrease ( 1.77%), colon weight increase (1.81±0.13), evident damage of the mucosa (MDA 526.94±80.34 mm 2 ) and increase of macroscopic damage score (MDS 5.90±0.316). Rifamycin SV at all the tested doses induced evident ( 32.4%, 33.2%, 41.5%) and significant (p = 0.015, p = 0.002, p = 0.006) reduction of the MDA. The MDS was significantly reduced ( 25.4%, p = 0.006) only at the higher dose, whereas the colon weight was significantly reduced ( 13%, p = 0.038) only by the lower dose. As expected, the intraperitoneal treatment with 0.2 mg of dexamethasone induced a significant reduction ( 20.3%, p = 0.032) of mucosal damage area, a significant colon weight reduction ( 23.2%, p < 0.005) and body weight loss ( 10.3%, p < 0.005) as compared with the vehicle treated group. Among tested cytokines, the percentage inhibition of IFNg production by the two concentrations of Rifamycin SV (10 9 M and 10 3 M) in ConA stimulated splenocytes was 10.4% and 46.9% at 48 h, and 54.2% and 77.6% at 72 h respectively. Results concerning other cytokines were not conclusive. Conclusions: The data herein reported showed that the oral administration of Rifamycin SV is able to ameliorate the local signs of DNB-induced colitis in rats. Moreover Rifamycin SV led to a significant reduction of IFNg in ConA-stimulated rat splenocytes. These results suggest a role of Rifamycin SV in intestinal diseases, not only as a broad-spectrum antimicrobial agent useful in infections, but also as an effective anti- inflammatory agent in the treatment of bowel inflammations, if administered directly in digestive tract. P309 Altered imprinting of lymphocyte homing by colonic dendritic cells in human ulcerative colitis S.C. Ng 1 *, R. Rigby 1 , A.L. Hart 1 , S. Plamondon 1 , N. Gellatly 2 , N.E. McCarthy 1 , H. Omar Al-Hassi 1 , M.A. Kamm 1 , S.C. Knight 1 , A.J. Stagg 2 . 1 Antigen Presentation Research Group, St Mark’s Hospital, London, United Kingdom, 2 Barts and Royal London Hospital, London, United Kingdom Background and Aims: Dendritic cells (DC) imprint homing patterns on T cells they activate. Murine CD103+ intestinal DC upregulate gut homing receptors a4b7 intergrin and CCR9 via the production and release of retinoic acid (RA). To test whether DC imprinting is dysregulated in human inflammatory intestinal disease, the expression of tissue-specific homing receptors on T cells activated by colonic DC from healthy subjects and ulcerative colitis (UC) patients was examined. Methods: Multi-colour flow cytometry was used to measure expression of homing markers on CD4+ T cells, following activation in the presence or absence of DC, and on ex vivo lymphocyte and antigen presenting cell populations in patients with UC (26) and controls (36). Results: Homing marker expression on human T cells was upregulated by activation in the absence of DC. RA increased expression of the intestinal homing integrin b7 and down- regulated skin homing receptors (CLA, CCR4). Colonic DC induced higher levels of intestinal homing b7 than peripheral blood DC. Colonic DC were highly stimulatory and subsets of responding T cells expressed b7, CLA and CCR4. However, b7 expression was greater on T cells activated by colonic DC from UC patients than on T cells activated by DC from healthy controls. DC expressing CD103 were significantly reduced in UC patients, possibly as a result of increased migration from the tissues. A subset of blood myeloid cells were b7+CD103 and may be precursors of gut tissue DC. Conclusions: Colonic DC from UC patients substantially increase T cell expression of b7 integrin. This early step in the recruitment of inflammatory cells may be a valuable therapeutic target. P310 The effect of infliximab treatment on angiogenic factors levels in patients with inflammatory bowel disease A. Algaba 1 *, P.M. Linares 2 , I. Domínguez 2 , I. de Pousa 2 , F. Bermejo 1 , J.P. Gisbert 2 , J.L. Rodríguez 1 . 1 Fuenlabrada University Hospital, Fuenlabrada, Spain, 2 La Princesa University Hospital, Madrid, Spain Aims: Infliximab (IFX) is a chimeric monoclonal antibody against TNFa effective in the treatment of Inflammatory Bowel Disease (IBD). Effectiveness of this drug could be related to the modification of different angiogenic proteins, such as some members of Vascular Endothelial Growth Factor gene family (VEGF and PlGF), angiopoietins (Ang-1 and Ang-2) and their receptor (Tie-2). Different studies reveal an increase of VEGF serum concentrations in patients with Crohn’s disease (CD) in comparison with healthy controls. There is only a survey in which a decrement of the VEGF serum concentrations has been observed in the patients with CD after IFX infusion. Our aim was to compare the concentrations of these angiogenic proteins in patients with IBD and healthy controls and to analyze their modifications during the treatment with IFX. Methods: Prospective and case-control study in 30 healthy controls and 12 patients with IBD that initiate treatment with IFX in induction + maintenance therapy. One serum sample was obtained from each control and 4 from each patient with IBD coinciding with the previous moments to the first 4 doses of IFX (week 0, 2, 6, and 14). VEGF, PlGF,Ang1,Ang2 and Tie2 serum concentrations were determined by ELISA. Results: Mean age in controls was 43±13 years, 50% men. Of the 12 patients with IBD, 11 were diagnosed as having CD and 1 had Ulcerative Colitis; mean age in this group was 35.4±8 years, 75% women, 50% smokers and 50% in concomitant treatment with corticoids and azathioprine. In all cases there was response to IFX treatment (CDAI/Truelove- Witts). Patients with IBD had significantly higher concentrations of Ang-2 (p = 0.001) and their receptor, Tie-2 (p = 0.000) than controls. No significant differences were found for the rest of proteins. In patients with IBD a tendency to lower values of Ang-1 than those of the controls was observed. Concentrations of VEGF, PlGF, Ang-1, Ang-2 and Tie-2, were unchanged during treatment with IFX. VEGF (pg/ml) PlGF (ng/ml) Ang-1 (ng/ml) Ang-2 (ng/ml) Tie-2 (ng/ml) Healthy controls 335±118 23±9 67±23 3.9±2.0 22±7 Pre treatment 333±206 21±10 56±17 8.7±5.6* 80±46* Week 2 231±159 19±7 55±19 8.1±6.5 73±47 Week 6 284±206 17±6 49±19 8.0±4.7 74±47 Week 14 321±221 18±6 45±17* 8.1±4.4 70±41 *Significant values (p < 0.05) respect to healthy controls. Conclusions: 1. There are significant differences of Ang2 and Tie2 serum concentrations between patients with IBD and healthy controls. Downloaded from https://academic.oup.com/ecco-jcc/article-abstract/3/1/S132/2393911 by guest on 12 June 2020