Portal de Periódicos da CAPES

Ueg Week 2020 Poster Presentations

2020; Wiley; Volume: 8; Issue: S8 Linguagem: Inglês

10.1177/2050640620927345

2050-6414

Helicobacter pylori-related gastroenterology studies

United European Gastroenterology JournalVolume 8, Issue S8 p. 144-887 UEG Week 2020 Poster PresentationsOpen Access Ueg Week 2020 Poster Presentations First published: 01 October 2020 https://doi.org/10.1177/2050640620927345Citations: 2AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat P0001 Serum Adipokines As Non-Invasive Biomarkers in Crohn's Disease Moreno L. Ortega1, 2, A. Sanz-Garcia3, M.J. Fernandez de la Fuente4, R. Arroyo Solera5, S. Fernández-Tomé1, A.C. Marin1, 6, I. Mora-Gutierrez1, P. Fernández5, M. Baldan-Martin1, 6, M. Chaparro Sanchez1, 2, 6, D. Bernardo1, 6, 7, J. Gisbert1, 2, 6 1Hospital de La Princesa, Gastroenterology, Madrid, Spain 2Universidad Autonoma de Madrid, Medicine, Madrid, Spain 3Hospital de La Princesa, Unidad de Analisis de Datos, Madrid, Spain 4Universidad de Alcala, Farmacia, Madrid, Spain 5Instituto de Medicina Molecular Aplicada (IMMA). Universidad San Pablo CEU, Medicine, Madrid, Spain 6Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain 7Instituto de Biología y Genética Molecular (IBGM). Universidad de Valladolid-CSIC, Valladolid, Spain Contact E-Mail Address: lorena.ortega8317@gmail.com Introduction Adipose tissue wrapping the gastrointestinal tract is a risk factor for disease activity in Crohn's disease (CD). Indeed, adipokines associated to lipid metabolism can modulate local immune responses. However, few studies have investigated the possible association between adipokines and CD. Aims & Methods Here, we aimed to evaluate the role of serum adipokines as possible biomarkers in CD. Serum samples were obtained from 18 patients with endoscopically active CD (aCD), 22 patients with endoscopically quiescent CD (qCD) and 36 non-inflamed healthy controls (HC). All serum samples were obtained from CD patients and HC at the moment of colonoscopy in Hospital Universitario La Princesa, Madrid, Spain. The Simple Endoscopic Score for Crohn's Disease (SES-CD) was determined during colonoscopy in all CD patients in order to classify them as aCD (SES-CD 3 3) or qCD (SES-CD ≤ 2). Demographic variables (i.e. sex, age and BMI) were analysed by chi square test (frequencies) or ANOVA test (means). Serum leptin, ghrelin, resistin and adiponec-tin were analysed by Multiplex (Bio-Rad, Hercules, CA, USA) in a Luminex 200 system technology following manufacturer's instructions. The final concentration value of each adipokine was the result of the mean from the two duplicated measures. Adipokines normality was tested and adipokines were natural log transformed. Spearman correlation was performed for the adipokines. Adipokine means for each group of patients were compared by ANOVA test. Median and interquartile range for each patient group was determined for those skewed adipokines and Kruskal-Wallis test was performed. Receiver Operating Characteristic (ROC) curves and the area under the curve (AUC) were carried on to evaluate the discriminatory capacity of the adipokines levels between study groups. The Youden cut-off index got from the ROC curve was matched with the adipokines concentration. Furthermore, for those adipokines that showed an AUC ≥ 0.7, a binary logistic regression adjusted by possible confounders (i.e sex, age, BMI) was performed in order to test their possible association with CD. Results No differences were found in age, sex or BMI among aCD, qCD and HC. There was no correlation among the adipokines analyzed. Means distribution for serum resistin was different among aCD, qCD and HC (p=0.02). However, only comparisons between aCD and HC a groups showed significant differences (p=0.03) in the post hoc test. Serum leptin, ghrelin and adiponectin did not show differences between means. ROC curve for resistin showed an AUC along with its 95% confidence interval of 0.75 (0.61-0.89) when HC and aCD groups were compared. Furthermore, in this case, as sensitivity and specificity for Youden index correspond to the total resistin median concentration (9822pg/ml), this value was selected as a cut-off for the binary logistic regression analysis; thus, odds ratio (OR) along with their 95% confidence interval analysis of high relative resistin levels (values higher than total resistin median) adjusted by age, sex and BMI yielded a value of 5.46 (1.34-22.14) when active patients were compared to HC. Comparisons between qCD and aCD or between qCD and HC showed an AUC < 0.7. ROC curves analysis for leptin, ghrelin and adiponectin did not show enough accuracy to discriminate between groups. Conclusion Resistin may modulate the inflammation state in CD and it is probably associated to activity, being this association independent of sex, age or BMI. Resistin may work as a serum biomarker of activity in CD. Disclosure Nothing to disclose P0003 Redefining Patterns of Tumour Response To Chemoradiotherapy in Oesophageal Cancer with The Aid of Ai Martínez C. Graham1, A. Al-Kaabi2, T. Strausz1, J.M. Bokhorst3, C. Rosman4, P.D. Siersema2, I.D. Nagtegaal1, C. van der Post1 1Radboud University Medical Centre, Pathology, Nijmegen, Netherlands 2Radboud University Medical Centre, Gastroenterology and Hepatology, Nijmegen, Netherlands 3Radboud University Medical Centre, Computational Pathology, Nijmegen, Netherlands 4Radboud University Medical Centre, Surgery, Nijmegen, Netherlands Contact E-Mail Address: cristina.grahammartinez@radboudumc.nl Introduction Tumour response has been categorized in many ways with-in-and-between tumour types. in order for tailored treatment decisions to be made, there is a need for a reproducible, objective and standardized assessment of response which combines histological patterns and down-staging. Aims & Methods Our cohort was composed of 100 patients with oesophageal adenocarcinoma (cT2-T3) treated with chemoradiotherapy. Three H&E slides per patient were analysed by a panel of pathologists and run through an algorithm to determine tumour cell percentage (TC%), size and distance between tumour fragments. Clinical data was used to determine correlations to survival and recurrence. Results Four histological patterns of regression were distinguished; fragmented (clustered or scattered), shrinkage and no-response. TC% was found to be significantly higher in clustered fragmentation subtype compared to scattered subtype in the mucosa (p=0.04) and tended to be higher in submucosa (p=0.08), muscularis (p=0.15) and subserosa (p=0.32). Preliminary results were obtained with only 70 patients, which we hope to increase to 100. Conclusion By using trained algorithms it is possible to accurately determine subtypes of patterns of response in an unbiased approach which might form the basis of predictive biomarker research. Recognition of these patterns of response and correlation with clinical outcome could provide a useful prognostic marker for further treatment. Moreover, our algorithms might be transferable to other cancer types. Disclosure Nothing to disclose P0004 Significance of Estrogen Receptor Expression in Esophageal Adenocarcinoma: Proof of Concept A. Mokrowiecka1, E. Malecka-Panas1, D. Jacenik2 1Medical University of Lodz, Department of Digestive Tract Diseases, Lodz, Poland 2University of Lodz, Department of Cytobiochemistry, Lodz, Poland Contact E-Mail Address: anna.mokrowiecka@umed.lodz.pl Introduction Estrogens play a crucial role in the development and progression of multiple types of cancer. Estrogen signaling through nuclear estrogen receptors (ERs), i.e. ERa and ERβ as well as membrane-bound estrogen receptor, i.e. G protein-coupled estrogen receptor (GPER), participates in the regulation of cancer cell proliferation and migration. However, the importance of estrogen receptors in esophageal adenocarcinoma is elusive. Aims & Methods To better assess the significance of estrogen receptors in esophageal adenocarcinoma, bioinformatic analysis was performed using datasets provided by Global Expression Omnibus and The Cancer Genome Atlas Esophageal Carcinoma from The Cancer Genome Atlas. Gene expression correlation was carried out with the Genevestigator co-expression tool. Pathway enrichment was evaluated with The Kyoto Encyclopedia of Genes and Genomes pathway using functional annotation of The Database for Annotation, Visualization and Integrated Discovery. Survival analysis was determined with Kaplan-Meier plotter. Results Gene expression profiling of estrogen receptors using dataset from Global Expression Omnibus revealed deregulation of ERa, ERβ and GPER expression in esophageal adenocarcinoma. Pathway enrichment analysis confirmed that estrogen receptors are correlated with genes participated in metabolic pathways, S. aureus infection, complement and coagulation cascades, oxidative phosphorylation, neurodegenerative diseases, spliceosome and ribosome biology as well as RNA transport. The Kaplan-Meier analysis documented poor overall survival in esophageal carcinoma patients with lower expression of ERa. in contrast, lower expression of GPER seems to be associated with better overall survival in esophageal adenocarcinoma patients. Conclusion In the present study, we found alterations of estrogen receptors expression and a relationship between the level of estrogen receptors and genes involved in numerous essential processes in the neoplastic transformation of esophagus. Moreover, our analysis highlighted prognostic significance of ERa and GPER expression in esophageal adenocarcinoma patients. These findings point to the need of a better understanding on the role exerted by estrogen receptors in esophageal adenocarcinoma. Disclosure Nothing to disclose P0005 Mitochondria-Targeting Hydrogen Sulfide-Releasing Ap-39 in Prevention of Chemically-Induced Gastric Mucosal Damage D. Bakalarz1, 2, D. Wójcik1, M. Surmiak3, E. Korbut1, T. Brzozowski1, K. Magierowska1, M. Szetela1, M. Whiteman4, M. Magierowski1 1Jagiellonian University Medical College, Department of Physiology, Cracow, Poland 2Institute of Forensic Research, Department of Forensic Toxicology, Cracow, Poland 3Jagiellonian University Medical College, Department of Internal Medicine, Cracow, Poland 4University of Exeter, Exeter, United Kingdom Contact E-Mail Address: dominik.bakalarz@uj.edu.pl Introduction Hydrogen sulfide (H2S) is an endogenous gaseous mediator produced by L-cysteine metabolism due to the activity of particular enzymatic pathways. This molecule has been shown to affect mitochondrial complexes and in result to modulate anti-oxidative mechanisms. Interestingly, H2S-releasing pharmacological tools were shown to play a key role within digestive system pathophysiology exerting anti-inflammatory and anti-oxidative activity. Taking into account the experimental data, beneficial effects of H2S is strictly dose-dependent and the controlled release of this molecule seems to be crucial to avoid cytotoxicity and to obtain desired biological effects. Thus, we aimed to assess the effect of mitochondria-targeting H2S-releasing compound, AP-39 administered i.g. against the development of aspirin- or ethanol-induced GI damage. Aims & Methods Wistar rats were pretreated with vehicle, AP-39 (0.004-2.5 mg/kg i.g.) or NC-AP-39 as structural control to AP-39 without ability to release H2S. After 30 min, gastropathy was induced by aspirin (125 mg/ kg i.g.) or 75%-ethanol (1.0 ml, i.g.). Gastric lesions area and gastric blood flow (GBF) were determined by planimetry, histology and laser flowmetry, respectively. Gastric mucosal mRNA expressions of COX-1, COX-2, iNOS, annexin-A1 and TGF-β1 as well as serum contents of TGF-β1, TGF-β2, and TGF-β3 were determined by real-time PCR or Luminex platform, respectively. Gastric mucosal PGE2 content was determined by ELISA. Results Pretreatment with AP-39 (0.02 mg/kg i.g.) reduced gastric damage area induced by both, aspirin or ethanol with accompanied increased in GBF level. AP-39 decreased upregulated gastric mucosal mRNA expression for pro-inflammatory iNOS and maintained upregulated mRNA expression for anti-inflammatory annexin-A1 in gastric mucosa exposed to aspirin or ethanol. AP-39 decreased serum concentration of TGF-b1 and TGF-b2 but did not affect PGE2 content in gastric mucosa administered with aspirin or ethanol. NC-AP-39 did not prevent gastric mucosa in tested experimental models. Conclusion We conclude that mitochondria-targeting and H2S-releasing AP-39 applied i.g. exerts gastroprotective effect dose-dependently affecting gastric microcirculation. This compound seems to be promising for the further studies related to the role of hydrogen sulfide in regulation of mitochondrial complexes activity in pathophysiology of GI tract. Disclosure Nothing to disclose 10.1177/2050640620927345 P0006 Tracking The Somatic Gastric Cancer Tissue Mutations in The Blood: Proportion of The Patients with Detectable Alterations and Association with Oncoproteins G. Streleckiene1, M. Forster2, K. Balciute1, J. Kupcinskas3, L. Kupcinskas1, 4, J. Skieceviciene1 1Lithuanian University of Health Sciencies, Institute for Digestive Research, Kaunas, Lithuania 2Christian-Albrechts-Universität zu Kiel, Institute of Clinical Molecular Biology, Kiel, Germany 3Lithuanian University of Health Sciencies, Department of Gastroenterology, Kaunas, Lithuania 4Kaunas, Department of Gastroenterology, Kaunas, Lithuania Contact E-Mail Address: greta.streleckiene@gmail.com Introduction Gastric cancer (GC) is one of the most common and lethal oncological diseases of the gastrointestinal tract worldwide (Ferlay et al. 2015). Determination of specific and individual molecular multi-layer “signatures” has been shown to be pivotal for prediction, diagnosis and monitoring of various cancers, with implications for precision medicine (Cohen et al. 2018). Since the discovery of the circulating plasma cell-free DNA (cfDNA) the origin and characteristics of cfDNA were extensively studied. It was shown that cfDNA could harbour genetic aberrations from malignant tissue. However, there is a lack of comprehensive studies conducted in GC. Aims & Methods GC tissue and blood were collected from 30 patients who were recruited at the Department of Gastroenterology, Lithuanian University of Health Sciences Hospital. Tumour tissue samples were obtained from the primary lesion of the resected specimen or biopsy and stored at -80 °C as a fresh-frozen sample. Peripheral blood was drawn at admission (before surgery), centrifuged and stored at -80 °C until DNA isolation. Genomic DNA form primary lesion was isolated using Qiagen miRNeasy Mini kit and DNA from white blood cells (WBC) was isolated using salting-out method. Total circulating nucleic acids from plasma were extracted using column based QIAamp Circulating Nucleic Acid isolation kit according to the manufacturers’ protocol. Whole exome sequencing (WES) was performed for GC patients’ tissue and paired WBC samples using IDT xGen Exome Research Panel and pair-end sequenced (2 x 100 bp) on NovaSeq 6000 platform. Targeted NGS using IDT xGen Custom Panel consisting of 38 gastric cancer-associated genes selected according WES results was performed for GC plasma cfDNA only. cfDNA libraries were pair-end sequenced (2 x 150 bp) on NovaSeq 6000 platform. Serum level of oncoproteins (CEA, CA19-9 and CA72-4) was measured with enzyme-linked immunosorbent assay (ELISA) in patients’ serum upon admission to the hospital. Results After WES was performed for GC tissue and normal WBC samples, in total for 23 of 30 patients (76.7 %) mutations associated with GC were determined. The most frequently mutated genes in our study were TP53, FAT4, GLI3,APC, KMT2C, SYNE1, EPHB1, PIK3CA, and TRRAP. Matching tissue and cfDNA alterations were detected for 14 of 23 (60.9 %) GC patients. A total of 121 variants in cell-free DNA, 202 variants in tumour samples and 40 matching alterations were detected. Tissue matching alterations in plasma were detected in genes: TP53, ERBB2, FAT1, MLH1, FAT4, SPEN, KMT2C, MUC16, ACVR2A, ERBB4, PREX2, and SYNE1. Matching tumour and plasma alterations were detected significantly more often in samples of the patients with larger tumours (55.6 % and 10.0%, T3-T4 and T1-T2 respectively, p=0.018). Number of detected alterations moderately correlated with age (R=0.38, p=0.048; R=0.47, p=0.012; and R=0.40, p=0.035; respectively number of matching alterations; tissue and plasma alterations). Specific mutations and levels of oncoproteins were analysed for discriminating T and M status. Levels of CEA correlated with total cfDNA yield (R=0.38, p=0.041) and was observed in higher levels for poorly differentiated ad-enocarcinoma cases (p=0.045). Conclusion Our results show, that tissue and cfDNA matching mutations were mostly detected for GC patients with larger tumours and in combination with different molecular analytes may enable cfDNA analysis for monitoring of the GC patients’ disease state. Disclosure Nothing to disclose References 1Ferlay Jacques et al. 2015. “Cancer Incidence and Mortality Worldwide: Sources, Methods and Major Patterns in GLOBOCAN 2012.” International Journal of Cancer 136(5): E359– 86. 2Cohen Joshua D. et al. 2018. “Detection and Localization of Surgically Resectable Cancers with a Multi-Analyte Blood Test.” Science 359(6378): 926– 30. P0007 Leukaemia Inhibitory Factor Signalling For Targeting Cancer Stem Cells in Gastric Adenocarcinoma L. Seeneevassen1, J. Giraud1, S. Molina-Castro2, E. Sifré1, C. Tiffon1, C. Beauvois1, C. Staedel3, F. Megraud1, 4, P. Lehours1, 4, O. Martin1, H. Boeuf5, P. Dubus1, 4, C. Varon1 1University of Bordeaux, Inserm U1053, Bordeaux, France 2University of Costa Rica, INISA School of Medicine, San José, Costa Rica 3University of Bordeaux, Inserm U 1212, Bordeaux, France 4CHU de Bordeaux, Bordeaux, France 5University of Bordeaux, Inserm U 1026, Bordeaux, France Contact E-Mail Address: lornella.seeneevassen@u-bordeaux.fr Introduction Cancer stem cells (CSCs) present intrinsic chemo-resistance mechanisms contributing to tumour maintenance and recurrence, making their targeting of utmost importance in cancer therapy. The Hippo pathway has recently been implicated in gastric CSC properties. and some studies have shown that it can be regulated by Leukaemia Inhibitory Factor Receptor (LIFR) and its ligand LIF. Interestingly, the impact of LIF on gastric CSCs has never been investigated. Consequently, this study aimed to determine the effect of LIF on CSC phenotype and properties in GC cell lines and patient derived xenograft (PDX) cells. Aims & Methods RTqPCR, 3D tumoursphere assays as well as immunofluorescence analysis were used to decipher the effect of LIF treatment on gastric CSC markers expression, tumoursphere formation and regulation of the Hippo pathway and LIF/LIFR canonical JAK/STAT pathway were evaluated. Results Results indicate that LIF treatment decreased gastric tumorigenic and chemo-resistant CSC population, in both GC cell lines and PDX cells. in addition, LIF increased activation of LATS1/2 Hippo kinases thereby decreasing downstream YAP/TAZ nuclear accumulation, TEAD transcriptional activity and target gene expression. LIF anti-CSC effect was reversed by Hippo kinase inhibition but not by JAKSTAT inhibition, highlighting the opposite effects of these two pathways downstream LIFR. Conclusion In conclusion, this study shows for the first time that LIF displays anti-CSC properties in GC and relates this effect to the activation of Hippo kinases LATS1/2. LIF treatment could in fine constitute a new CSCs-targeting strategy to help decrease relapse cases and bad prognosis in GC. Disclosure Nothing to disclose P0008 Can Neutrophil-To-Lymphocyte Ratio (Nlr) Be A Simple Predictive Marker For Gastric Intestinal Metaplasia? U. Kutluana1 Pamukkale University Medicine Faculty, Internal Medicine and Gastroenterology, Denizli, Turkey Contact E-Mail Address: drufukkanas@gmail.com Introduction Gastric intestinal metaplasia (GIM) and gastric atrophy (GA) are pre-neoplastic lesions that can lead to gastric cancer (GC). The diagnosis of GIM and GA usually based on endoscopic and histopathological findings (1). Nowadays, there are no recognized good biomarkers of GIM and GA. The neutrophil-to-lymphocyte ratio (NLR) is an economical, effective, and repetitive indicator of inflammation (2). in this study, we aimed to comparatively evaluate red cell distribution width (RDW) and NLR values in cases with GIM, GA and chronic gastritis, and to show the increased NLR in GIM. Aims & Methods 88 patients with GIM and 48 patients with GA and 64 patients with non-atrophic non-metaplastic gastritis were included in the study. NLR and RDW levels were measured in patients and controls. Results NLR levels were significantly higher in patients with GIM than in controls (p < 0.05). There was no significant difference in NLR levels in patients with GA and controls. There was no significant difference in RDW levels between groups. NLR level was correlated positively with presence of GIM (p < 0.05), H.pylori presence in GIM and GA (p < 0.05), and menopause (p < 0.05). A multiple logistic regression analysis showed the presence of GIM was predictor for elevated NLR (p < 0.05). According to the ROC curve analysis, the best cut-off NLR value to differentiate between patients with GIM from GA and/or controls was ≥2.92 (p < 0.05). Conclusion NLR is significantly higher in patients with GIM. NLR can be an independent determinant factor for GIM. Disclosure We have no conflict of interest References 3Eshmuratov A., Nah J.C., Kim N., Lee H.S., Lee H.E., Lee B.H. et al. The correlation of endoscopic and histological diagnosis of gastric atrophy. Dig Dis Sci 2010; 55: 1364– 75. PMID: 19629687 4Sato Y., Gonda K., Harada M., Tanisaka Y., Arai S., Mashimo Y. et al. Increased neutrophil-to-lymphocyte ratio is a novel marker for nutrition, inflammation and chemotherapy outcome in patients with locally advanced and metastatic esophageal squamous cell carcinoma. Biomedical Reports 2017: 7; 79– 84. PMID: 28685065 P0010 An Inflammatory Tumour Microenvironment Is Associated with Poor Response To Neo-Adjuvant Chemoradiotherapy and Poor Prognosis in Oesophageal Adenocarcinoma W. Koemans1, J. van Dieren2, J. Van den Berg3, G. Meijer3, P. Snaebjornsson3, M. Chalabi4, F. Lecot5, R. Riedl6, I. Hofland7, A. Broeks7, F. Voncken8, M. Sosef9, J. van Sandick1, L. Kodach10 1Netherlands Cancer Institute, Surgical Oncology, Amsterdam, Netherlands 2Netherlands Cancer Institute, Gastroenterology, Amsterdam, Netherlands 3Netherlands Cancer Institute, Pathology, Amsterdam, Netherlands 4Netherlands Cancer Institute, Gastrointestinal Oncology, Amsterdam, Netherlands 5Zudyerland Hospital, Surgery, Heerlen, Netherlands 6Zuyderland Hospital, Pathology, Heerlen, Netherlands 7 Netherlands Cancer Institute, Core Facility, Molecular Pathology and Biobanking, Amsterdam, Netherlands 7Netherlands Cancer Institute, Radiotherapy, Amsterdam, Netherlands 9Zuyderland Hospital, Surgery, Heerlen, Netherlands 10Netherlands Cancer Institute, Amsterdam, Netherlands Contact E-Mail Address: w.koemans@nki.nl Introduction Oesophageal adenocarcinomas (OAC) are relatively unresponsive to neo-adjuvant chemoradiotherapy (nCRT). The mechanism of a poor response to nCRT is not yet understood. One critical factor in the (non-)responsiveness to nCRT might be an immunosuppressive tumour microenvironment (TME). in this study, TME characteristics associated with a poor response to nCRT in OAC patients were investigated. Aims & Methods To study TME characteristics post-nCRT surgical resection specimens from 123 OAC patients and pre-nCRT biopsies from 42 patients were analysed using immunohistochemistry for immune cell subsets. The association between TME parameters and response to nCRT was studied, as well as the association between TME parameters and patient survival. in addition, characteristics in pre-nCRT and post-nCRT samples were compared. Results Non-responsive tumours showed a higher immune infiltrate density compared to responsive tumours in post-nCRT tumour samples, with a higher density of CD3+ T-cells (p< 0.001), CD8+ T-cells (p=0.001), FOXP3+T-cells (p=0.02) and CD20+ B-cells (p=0.006) (Table 1). The ratio between the different subsets of immune cells was not different between responders and non-responders. Non-responders showed more frequently PD-L1 expression compared to responders (59% versus 23%, p< 0.001). A high CD8 T-cell infiltration was significantly associated with a worse patient survival compared to a low CD8 T-cell infiltration. The PD-L1 status was discordant between pre- and post-CRT samples in 15 of 40 (38%) patients. [Table 1] Responders n=62 Non-responders n=61 p-value mean CD3+ count/mm2 1324 2370 <0.001 mean CD4+ count/mm2 442 827 <0.001 mean CD8+ count/mm2 641 1126 0.001 mean FOXP3+ count/mm2 182 261 0.024 mean CD20+ count/mm2 416 717 0.006 CD8+/CD3+ ratio 0.51 0.46 0.93 FOXP3+/CD3+ ratio 0.14 0.13 0.10 PD-L1 expression* negative 46 77% 25 41% <0.001 positive 14 23% 36 59% Conclusion Following results of this study, an ‘immune-inflamed pheno-type’ and an immunosuppressive TME identify OAC patients refractory to nCRT, suggesting that immunotherapy may be a valuable alternative or additional treatment option for this group of patients. Disclosure Nothing to disclose P0011 Anti-Inflammatory Effect of Ev (Extracellular Vesicles) Isolated From Bifidobacterium Breve in Raw264.7 Macrophage D.-H. Lee1, J.H. Kim2, Sung K. Ki2, C.-M. Shin3, H. Yoon4, Y.S. Park4, N. Kim4, E.J. Lee4, Y.J. Kim4 1Seoul National University Bundang Hospital, Division of Gastroenterology, Internal Medicine, Seoul, Korea (Republic of) 2BioBankHealing Inc, R&D Center, Seongnam, Korea (Republic of) 3Seoul National University Bundang Hospital, Internal Medicine, Seoul, Korea (Republic of) 4Seoul National University Bundang Hospital, Seoul, Korea (Republic of) Contact E-Mail Address: dhljohn@yahoo.co.kr Introduction Bifidobacterium breve (B. breve) secrete extracellular membrane vesicles (EV), which contain DNA, protein, and cell-wall components. EV is involved in microbiota-host cell communications in various biological systems. It was also reported EVs from B. breve can prevent intestinal inflammation through the induction of intestinal IL-10-producing Tr1 cells. in this study, we tested whether EV isolated from B. breve has an anti-inflammatory effect in LPS-induced inflammation. Aims & Methods B. breve was isolated from a human fecal sample, and it was cultured over 48 hours at 37°C under anaerobic conditions. After cultivation, the culture medium was centrifuged, subsequently, the supernatant was collected and concentrated. To measure whether the EV affects the viability of the Raw264.7 cell line, WST-1 analysis was used. NO (nitric oxide) concentration involved in immunity and inflammation was investigated in the cell line. ELISA was used to measure the production of inflammatory cytokine. Results The anti-inflammatory effect of EV isolated from B. breve was confirmed in Raw264.7 cell line. All experiments about EV treatment were under conditions of LPS-stimulation. When the pre-stimulated macrophages were treated with the EV, the concentration of NO, inflammatory factor, was significantly reduced than control. The EV (1ug/ml) treatment group (59.0±3.46 uM/L, p value vs positive = 0.012) had a 13% lower NO value than the positive control group (67.7±8.58 uM/L). It was also significantly reduced the TNF (tumor necrosis factor) level (40%, p value vs positive = 0.0029) of EV (1ug/ml) treatment group under the same conditions. However, IL-6 (interleukin-6) level (165%, p value vs positive = 0) which acts as both the anti-inflammatory factor and pro-inflammatory factor was increased. in this condition, cell viability was not different between EV treatment group and control group. Conclusion EV isolated from B. breve had an anti-inflammatory effect in the macrophage of inflammatory condition induced by LPS. These results suggested the potential that just EV alone without whole live form probi-otics could help suppress the inflammation. Disclosure Nothing to disclose P0012 A Risk-Based Diagnostic Algorithm Optimizes The Management of Caustic Intake Pardo A.M. Sánchez1, J. Tosca1, R. Villagrasa1, A. Sanahuja1, B. Herreros2, I. Pascual-Moreno1, M.P. Mas Mercader1, M. Minguez Pérez1 1Hospital Clinico Universitario de Valencia, Valencia, Spain 2Hospital Marina Baixa, Alicante, Spain Contact E-Mail Address: ana5.medicina@gmail.com Introduction Caustic ingestion is a potentially severe condition and identifying patients with a worse prognosis is essential to guide the treatment. Some authors recently proposed the use of computed tomography (CT) as the first test after every caustic intake, instead of endoscopy (1); however, these studies are based on samples from severe patients and their conclusions may not be completely inferred to the general population. An optimal diagnostic algorithm, based on the analysis of the different prognostic markers, would allow to detect severe cases and reduce the number of diagnostic tests. Aims & Methods Aims To identify risk factors for poor evolution of caustic intake in or