HIV progression is characterized by immune activation and microbial translocation. One factor that may be contributing to HIV progression could be a dysbiotic microbiome. We therefore hypothesized that the GI mucosal microbiome is altered in HIV patients and this alteration correlates with immune activation in HIV. 121 specimens were collected from 21 HIV positive and 22 control human subjects during colonoscopy. The composition of the lower gastrointestinal tract mucosal and luminal bacterial microbiome was characterized using 16S rDNA pyrosequencing and was correlated to clinical parameters as well as immune activation and circulating bacterial products in HIV patients on ART. The composition of the HIV microbiome was significantly different than that of controls; it was less diverse in the right colon and terminal ileum, and was characterized by loss of bacterial taxa that are typically considered commensals. In HIV samples, there was a gain of some pathogenic bacterial taxa. This is the first report characterizing the terminal ileal and colonic mucosal microbiome in HIV patients with next generation sequencing. Limitations include use of HIV-infected subjects on HAART therapy.

Inflammatory bowel disease (IBD) is a waxing and waning disease characterized by diarrhea, abdominal pain and weight loss. Recently, there has been an increased interest in the roles that sleep, circadian rhythms and melatonin could have as regulators of inflammation in the Gl tract. Advances in our understanding of the molecular machinery of the circadian clock, and the discovery of clock genes in the GI tract are opening up new avenues of research for a role of sleep in IBD. Altering circadian rhythm significantly worsens the development of colitis in animal models, and preliminary human studies have shown that patients with IBD are at increased risk for altered sleep patterns. Further research is needed to clarify the role of disturbances in IBD.Keywords circadian rhythms; Crohn's disease; inflammatory bowel disease; melatonin; sleep; ulcerative colitis Ulcerative colitis (UC) and Crohn's disease (CD) are the two phenotypic patterns of inflammatory bowel disease (IBD) [1]. CD has a transmural pattern of inflammation that can occur anywhere in the GI tract (GIT) and is associated with the development of complications such as fistulas or strictures [2]. UC has a superficial inflammation that occurs only in the colon. This inflammation begins in the rectum and is usually limited to the left side of the colon but with time may extend over the entire colon [3]. Currently, over 2 million people in the USA are diagnosed with IBD and the last several decades have seen an increasing incidence of the disease [4]. IBD has a waxing and waning course with periods of asymptomatic remission interrupted with episodes of disease 'flare' where patients can present with bloody stools, diarrhea, fever and abdominal pain.Currently the etiology of IBD is not known and thus it is not surprising that there is no cure for IBD; the primary treatment goal is to improve patients' quality of life by treating flare ups and maintaining remission. The most effective approach to maintaining remission is to †

OBJECTIVES:Bowel preparations (BPs) taken before colonoscopy may introduce a confounding effect on the results of gastrointestinal microbiota studies. This study aimed to determine the effect of bowel preparation on the mucosa-associated and luminal colonic microbiota in healthy subjects (HC) and inflammatory bowel disease (IBD) patients.METHODS:Biopsy samples (n=36) and fecal samples (n=30) were collected from 10 HC and 8 IBD subjects pre- and post-BP. 16S rRNA gene was pyrosequenced using 454 Titanium protocols. We compared the differences between the pre- and post-BP samples (i.e., comparisons-across-bowel-prep); we examined the effect of BP on the expected separation of the mucosal vs. the luminal compartments (i.e., comparisons-across-compartments). Last, we compared the baseline differences between the HC vs. IBD groups (a secondary analysis), and examined whether the differences between the HC vs. IBD changed after BP.RESULTS:In comparisons-across-bowel-prep, the Shannon's index (SI) decreased only in the biopsy samples of IBD subjects post-BP (P=0.025) and phylogenetic diversity-whole tree (PD-WT) metric decreased in biopsy samples of HC subjects post-BP (P=0.021). In secondary comparisons, the subtle differences between the fecal samples of the HC vs. IBD groups, in terms of evenness and the SI, were not apparent post-BP. In terms of β-diversity, in comparisons-across-bowel-prep, the proportion of shared operational taxonomic units (OTUs) in pre- and post-BP samples was low (~30%) and unweighted Unifrac distances between pre- and post-BP specimens ranged from 0.52 to 0.66. HC biopsies were affected more than IBD biopsies with BP (P=0.004). In comparisons-across-compartments, the proportion of shared OTUs between biopsy and fecal samples increased and Unifrac distances decreased post-BP in IBD subjects, reducing the differences between the mucosal and luminal compartments of the gut microbiota. Interindividual differences in Unifrac distances were preserved even with BP effects, although the effects were greater on weighted Unifrac distances. Bacteroidetes and its subtypes increased post-BP in both the luminal and mucosal compartments.CONCLUSIONS:Bowel preparations affect the composition and diversity of the fecal and luminal microbiota in the short term, introducing potential bias into experiments examining the gut microbiota. The magnitude of the effect of BP is not greater than that of interindividual variation. Both the luminal and mucosal compartments of the gut microbiota get affected, and samples from controls and IBD subjects may get affected differently. Studies of the colonic microbiota should take into account the direction and the magnitude of the change introduced by BP during the design stage of the experiments, and consider sample sizes so that potential bias is minimized.

Gastroenterologists should recognize that IBD is more complex when presenting in adolescence and our data support the creation of specific adolescent transitional clinics.

Alcohol consumption is a potential trigger for flare in Inflammatory Bowel Disease (IBD) flare because of alcohol’s pro-oxidant effects and its deleterious effects on gut barrier function. The association with alcohol consumption and IBD flare is unclear. To test this hypothesis, we evaluated the pattern of alcohol consumption and its self-reported effect on gastrointestinal (GI) symptoms in patients with IBD. We recruited 129 consecutive patients: 52 patients with Crohn’s Disease, 38 patients with Ulcerative Colitis, and 39 patients with Irritable Bowel Syndrome (IBS). All participants completed a validated questionnaire on disease activity, the CDAI or UCAI respectively, validated questionnaires to quantify alcohol consumption by NIAAA criteria, and two structured questionnaires we designed to access patients’ perception of the effect of alcohol on their GI symptoms and on overall GI symptom severity. The pattern of current, light, moderate, and heavy alcohol consumption in inactive IBD was similar to the general US population. Specifically, 56 of 90 (62%) of inactive IBD patients were current drinkers, compared to 61% in the general US population. Of current drinkers, 75% of IBD (N=42), and 43% of IBS (N=9) reported a worsening of GI symptoms with alcohol consumption (p=0.01); however, overall GI symptom severity did not differ when compared to quantity of alcohol consumed. Patients with inactive IBD drink alcohol in quantities similar to the general population. Current drinkers with inactive IBD are more likely to report worsening of GI symptoms with alcohol than current drinkers with IBS.