AGA Abstracts explain the protective effect of this fiber. The aim of this study is to understand the effect of psyllium on the gut microbiota and study the consequences of these changes on host gene expression. Methods. 7-week-old mice were fed grain-based chow (GBC) or a composi- tionally defined diets (CDD) comprised of 20% total fiber, which was comprised of all cellulose or a 1:1 mixture of cellulose, inulin, psyllium, or resistant corn starch for a period of 4 weeks. Feces were collected before and 4 weeks after the diet intervention. Microbiota was analyzed using shotgun metagenomic sequencing and 16S qPCR. Colon gene expression at the 4 week time point, was assayed by RNAseq. Results. Contrary to other fermentable fibers, namely inulin and resistant corn starch, that increased gut bacterial density, psyllium dramatically reduced bacterial density in the colon and the feces. Metagenomic sequencing revealed that inulin partially restored microbiota composition toward that of mice fed GBC, whereas psyllium promotes a wholly unique microbiota as show by the clustering in PCoA analysis. Microbiota alteration of psyllium-fed mice was driven an increase in Proteobacteria such as Burkholeriales and Sutterellaceae and Firmicutes belonging to Erysipelotrichaceae and Clostridiaceae family and a decrease of the phylum Baceroidetes and Firmicute family Lachnospiraceae and Ruminococcaceae. RNAseq analysis showed that, compared to mice fed GBC, CDD induced a completely different profile of expression. Contrary to the other fibers, psyllium partially restored the colon gene expression profile toward mice fed GBC. Discussion. These results show that psyllium induced a unique effect on the microbiota composition that correlated with restoration of a healthy colonic gene expression profile thus potentially explaining how psyllium promotes gut and metabolic health and amelioration of severe gut inflammation. Tu1261 RESTRAINT STRESS INDUCES DEPRESSIVE-LIKE BEHAVIOR AND INCREASES COLONIC LYMPHOID AGGREGATE FORMATION IN A MOUSE MODEL OF CROHN’S DISEASE Adrian Gomez-Nguyen, Ludovica Butto, Abigail R. Basson, Kristen Hsu, Luc M. Dark, Theresa T. Pizarro, Fabio Cominelli Patients with Crohn’s disease (CD) suffer from abnormally high rates of depression and anxiety. Depression among patients with CD are higher than other debilitating chronic medical conditions, such as cancer. Behavioral co-morbidities are associated with increased rates of flares, more severe disease course, and increased rate of corticosteroid prescription. Psychological stress, even among CD patients in remission, is recognized as a risk factor for flare-ups. Despite the well-established relationship between stress and symptom relapse, a rigorous mechanistic explanation remains elusive. Here we demonstrate alterations in the behavioral profile and the mucosal immune system in the SAMP1/YitFc (SAMP1) mouse, a spontaneous model of CD-like ileitis, following exposure to acute and chronic psychological stress. Two separate experiments were performed to evaluate the impact of acute and prolonged restraint stress (RS) on our SAMP1 mice. For each experiment SAMP1 littermates were sex matched and divided into two groups (n = 5-8). Mice were restrained for 180 minutes per day in a 50mL conical tube with several air holes drilled for adequate ventilation. Acute RS mice were restrained for 7 consecutive days. Prolonged RS was performed for 56 consecutive days (8 weeks). Stool samples and weights were recorded regularly. Subsequently, each group was subjected to behavioral testing to determine anxiety-like behavior (open field and elevated plus maze), depressive-like behavior (tail suspension), motor deficits (line crossings and rota-rod), and cognitive deficits (Y-maze). Immediately after, mice were sacrificed and tissue samples were collected for immunological analysis. Mice subjected to both acute and prolonged RS displayed increased immobility time during tail suspension indicating a depressive-like phenotype (p < 0.05). All other behavioral characteristics remained unchanged compared to control. A trend of increased mesenteric lymph node (MLN) dendritic cells (DCs) was seen in both the acute and prolonged RS groups (p = 0.07 and p = 0.08 respectively). Mice subjected to prolonged RS, but not acute RS, developed a pronounced increase colonic growths. Histological staining revealed these growths to be large collections of lymphoid cells which we have termed, “stress-enhanced lymphoid aggregates” (SELAs). Further characterization of the SELAs is underway. The marked differ- ence in the MLN DC population is suggestive of abnormal luminal sampling of intestinal bacteria due to stress-induced dysbiosis. We hypothesize that the emergence of SELAs is a result of this dysbiosis. In addition to further investigating SELAs, characterizing the microbi- ome and its associated metagenome is a vital next step in our work. Colonic lymphoid aggregates were dramatically (p = 0.008) increased following chronic restraint stress. S-1036 AGA Abstracts Mice exhibited depressive-like behavior (tail suspension; p = 0.0264) following chronic restraint stress. Other behavioral parameters were unchanged. Tu1262 GUT MICROBIOME OF JAPANESE PATIENTS OF INFLAMMATORY BOWEL DISEASE Hitoshi Nakajima Background Dysbiosis of gut microbiome has been reported in the patients of inflammatory bowel disease (IBD). Gut microbiome of the healthy Japanese is known to be different from those of other populations. We conducted a cross-sectional study to characterize the gut microbiome of the Japanese patients of Crohn’s disease (CD) and ulcerative colitis (UC). Methods Two-hundred and eighty-four patients of IBD (39 with CD and 245 with UC) and 31 healthy participants were enrolled. The gut microbiome was analyzed by 16S rRNA amplicon sequencing using Illumina Miseq. Results There was a significant difference of gut microbiome between the patients of CD, the UC, and the healthy individuals. Species richness and evenness were significant lower in the active patients of IBD than the healthy individuals. At the genus level, Bifidobacterium was most abundant genera in the three groups. Pathogenic obligate anaerobes such as Prevotella and Veillonella increased and beneficial bacteria shch as Lachnospiraceae and Ruminococcaceae reduced. Conclusions The patients of CD and the patients of UC each had different gut microbiome with dysbiosis. However, characteristic feature of the gut microbiome with high abundance of the genus Bifidobacterium was main- tained in the Japanese patients of IBD. Disease activity affected gut microbiome in the patients of IBD. Tu1263 IMMUNOLOGICAL EVALUATION OF FECAL MICROBIOME TRANSPLANTED HELICOBACTER NEGATIVE MICE WITH SPONTANEOUS ILEITIS Luc M. Dark, Adrian Gomez-Nguyen, Ludovica Butto, Abigail R. Basson, Fabio Cominelli The Helicobactereraceae genus is commonly associated with H. Pylori, the causative organism behind peptic ulcer disease. Mouse models of intestinal inflammation are susceptible to confounding results between mice with an uncharacterized Helicobacter status. Reports have demonstrated pro-inflammatory effects from a key set of enterohepatic Helicobacter spp. Here we proposed a study to characterize the inflammatory profile in our model of spontaneous murine ileitis with variable Helicobacter colonization. The SAMP1/YitFc mouse, a spontaneous model of Crohn’s disease-like ileitis, were used for this study. We confirmed the Helicobacter colonization status of our mice using 16s rRNA sequencing. Blood collected by cardiac stick will be analyzed for cytokines. Flow cytometry was performed on spleen and MLN to characterize immune cell populations across groups. We had three groups of mice: A Helicobacter positive group, a helicobacter negative group, and a fecal microbiome transplanta- tion (FMT) oral gavage group ( helicobacter positive into helicobacter negative). Mice at three ages (10, 20, and 30 weeks) were sacrificed (n=10) for specimen collection. Severity of ileitis will be assessed by weight prior to sacrifice; histology and stereomicroscopy will be used to assess post-mortem ileitis. Our FACS data demonstrated significantly increased interdigitating dendritic cells, increased effector T cells, decreased memory T cells, and decreased non-interdigitating dendritic cells, and decreased weight in both Helicobacter positive and FMT groups. These findings suggest an overall increase in mucosal inflammation and luminal sampling, a shift towards the effector state, and an increase in adaptive immune response in our experimental groups. FACS data confirms our hypothesis that Helicobacter acts as insult to the immune system, stimulating an inflammatory response in Helicobacter positive and FMT groups. Tu1264 THE ROLE OF GASTROINTESTINAL PATHOGENS BY STOOL POLYMERASE CHAIN REACTION TESTING IN THE DEVELOPMENT OF INFLAMMATORY BOWEL DISEASE Sanskriti Varma, Peter H. R. Green, Suneeta Krishnareddy Introduction The luminal microbiome is linked to inflammatory bowel disease (IBD) and may be altered in the progression and flare of disease. It is unclear how the microbiome is implicated in IBD development. We sought to investigate the role of microbial pathogens in the development of IBD by means of stool gastrointestinal (GI) pathogen polymerase chain reaction (PCR) testing. Methods We performed a retrospective analysis, which included patients of all ages with a positive stool GIPCR test and subsequently a new documentation of ICD9/10 code for IBD (either Crohn’s disease [CD] or ulcerative colitis [UC]), from 2015 and onward at Columbia University Medical Center. The IBD diagnosis (dx) was confirmed by chart review and documented endoscopic and/or biopsy findings. Patients who had ICD9/ 10 codes specifying IBD dx prior to GIPCR study date were excluded. We collected baseline demographics and clinical factors. We then used descriptive statistics to characterize and