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Crohn’s disease (CD) results from a complex interplay between host genetic factors and endogenous microbial communities. In the current study, we used Ion Torrent sequencing to characterize the gut bacterial microbiota (bacteriome) and fungal community (mycobiome) in patients with CD and their nondiseased first-degree relatives (NCDR) in 9 familial clusters living in northern France-Belgium and in healthy individuals from 4 families living in the same area (non-CD unrelated [NCDU]). Principal component, diversity, and abundance analyses were conducted, and CD-associated inter- and intrakingdom microbial correlations were determined. Significant microbial interactions were identified and validated using single- and mixed-species biofilms. CD and NCDR groups clustered together in the mycobiome but not in the bacteriome. Microbiotas of familial (CD and NCDR) samples were distinct from those of nonfamilial (NCDU) samples. The abundance of Serratia marcescens and Escherichia coli was elevated in CD patients, while that of beneficial bacteria was decreased. The abundance of the fungus Candida tropicalis was significantly higher in CD than in NCDR ( P = 0.003) samples and positively correlated with levels of anti- Saccharomyces cerevisiae antibodies (ASCA). The abundance of C. tropicalis was positively correlated with S. marcescens and E. coli , suggesting that these organisms interact in the gut. The mass and thickness of triple-species ( C. tropicalis plus S. marcescens plus E. coli ) biofilm were significantly greater than those of single- and double-species biofilms. C. tropicalis biofilms comprised blastospores, while double- and triple-species biofilms were enriched in hyphae. S. marcescens used fimbriae to coaggregate or attach with C. tropicalis / E. coli , while E. coli was closely apposed with C. tropicalis . Specific interkingdom microbial interactions may be key determinants in CD. IMPORTANCE Here, we characterized the gut bacterial microbiota (bacteriome) and fungal community (mycobiome) in multiplex families with CD and healthy relatives and defined the microbial interactions leading to dysbiosis in CD. We identified fungal ( Candida tropicalis ) and bacterial ( Serratia marcescens and Escherichia coli ) species that are associated with CD dysbiosis. Additionally, we found that the level of anti- Saccharomyces cerevisiae antibodies (ASCA; a known CD biomarker) was associated with the abundance of C. tropicalis . We also identified positive interkingdom correlations between C. tropicalis , E. coli , and S. marcescens in CD patients and validated these correlations using in vitro biofilms. These results provide insight into the roles of bacteria and fungi in CD and may lead to the development of novel treatment approaches and diagnostic assays. Here, we characterized the gut bacterial microbiota (bacteriome) and fungal community (mycobiome) in multiplex families with CD and healthy relatives and defined the microbial interactions leading to dysbiosis in CD. We identified fungal ( Candida tropicalis ) and bacterial ( Serratia marcescens and Escherichia coli ) species that are associated with CD dysbiosis. Additionally, we found that the level of anti- Saccharomyces cerevisiae antibodies (ASCA; a known CD biomarker) was associated with the abundance of C. tropicalis . We also identified positive interkingdom correlations between C. tropicalis , E. coli , and S. marcescens in CD patients and validated these correlations using in vitro biofilms. These results provide insight into the roles of bacteria and fungi in CD and may lead to the development of novel treatment approaches and diagnostic assays.

Over the past decades, increasing interests took place in the realm of drug delivery systems. Beyond treating intestinal diseases such as inflammatory bowel disease, colon targeting can provide possible applications for oral administration of proteins as well as vaccines due to the lower enzymatic activity in the distal part of GIT. To date, many strategies are employed to reach the colon. This article encompasses different biomaterials tested as film coatings and highlights appropriate formulations for colonic drug delivery. A comparison of different films was made to display the most interesting drug release profiles. These films contained ethylcellulose, as a thermoplastic polymer, blended with an aqueous shellac ammonium salt solution. Different blend ratios were selected as well for thin films as for coated mini-tablets, mainly varying as follows: (80:20); (75:25); (60:40). The impact of blend ratio and coating level was examined as well as the addition of natural polysaccharide “inulin” to target the colon. In vitro drug release was measured in 0.1 M HCl for 2 h followed by phosphate buffer saline pH 6.8 to simulate gastric and intestinal fluids, respectively. Coated mini-tablets were exposed to fresh fecal samples of humans in order to simulate roughly colonic content. Several formulations were able to fully protect theophylline as a model drug up to 8 h in the upper GIT, but allowing for prolonged release kinetics in the colon. These very interesting colonic release profiles were related to the amount of the natural polysaccharide added into the system. Graphical Abstract

Abundant data have incriminated intestinal bacteria in the initiation and amplification stages of inflammatory bowel diseases. However, the precise role of intestinal bacteria remains elusive. One theory has suggested a breakdown in the balance between putative species of “protective” versus “harmful” intestinal bacteria—this concept has been termed “dysbiosis”. Arguments in support of this concept are discussed.

[...]other mediators such as angiotensinogen, plasminogen activator inhibitor-1 (PAI-1), visfatin, adisin and vaspin are produced by adipocytes. Local activation of PPAR[GAMMA] is more likely responsible for mesenteric fat hypertrophy in IBD patients. Besides dietary factors, PPAR[GAMMA] expression is modulated by several bacterial stimuli. 72 Given the epithelial barrier defects in Crohn's disease leading to an increased intestinal permeability and bacterial translocation, the intestinal flora may directly regulate the mass of mWAT.

The increasing incidence of inflammatory bowel diseases (IBDs) in developing countries has highlighted the critical role of environmental pollutants as causative factors in their pathophysiology. Despite its ubiquity and immune toxicity, the impact of aluminum in the gut is not known. This study aimed to evaluate the effects of environmentally relevant intoxication with aluminum in murine models of colitis and to explore the underlying mechanisms. Oral administration of aluminum worsened intestinal inflammation in mice with 2,4,6-trinitrobenzene sulfonic acid- and dextran sodium sulfate-induced colitis and chronic colitis in interleukin 10-negative (IL10−/−) mice. Aluminum increased the intensity and duration of macroscopic and histologic inflammation, colonic myeloperoxidase activity, inflammatory cytokines expression, and decreased the epithelial cell renewal compared with control animals. Under basal conditions, aluminum impaired intestinal barrier function. In vitro, aluminum induced granuloma formation and synergized with lipopolysaccharide to stimulate inflammatory cytokines expression by epithelial cells. Deleterious effects of aluminum on intestinal inflammation and mucosal repair strongly suggest that aluminum might be an environmental IBD risk factor.

OBJECTIVE: Bacterial agents have been implicated in the early recurrence of Crohn’s disease after ileocolectomy. The aim of our study was to identify and quantify bacteria associated with the ileal mucosa in patients and controls and to correlate specific bacteria with recurrence. METHODS: The predominant bacterial microflora of the ileum were enumerated and identified, aerobically and anaerobically, in biopsies obtained at the time of surgery or by endoscopy from 61 patients with Crohn’s disease and 10 ileocolectomy controls. The 61 specimens were comprised of 13 ileal biopsies taken from resection specimens, seven taken after ileostomy, and 41 taken after ileocolectomy. RESULTS: Ileocolectomy induced a significant increase in bacterial counts and variety in the neoterminal ileum in both patients and controls that was not observed in ileostomy biopsies. Comparison between patients and controls revealed greater numbers of Escherichia coli and enterococci in Crohn’s disease and of bifidobacteria and ruminococci in controls. Early recurrence was associated with high counts of E. coli and bacteroides and the frequent isolation of fusobacteria. CONCLUSION: After ileocolectomy, colonization of the neoterminal ileum is increased. Our data suggest that increases in the populations of specific bacteria such as E. coli, enterococci, bacteroides, and fusobacteria may be important in postoperative recurrence of Crohn’s disease.

A suggestion is made that this deficiency could be linked to increased proximal small intestinal permeability with enhanced absorption of prebiotic substrate, causing a relative deficit of prebiotics distally.

Digestive bacterial microflora play a major role in the pathogenesis of Crohn's disease (CD). Bacterial enzyme activities, especially beta-D-galactosidase, are decreased in fecal extracts from CD patients. We hypothesized that an alteration of the colonic flora might be responsible for this decrease. Indeed, we demonstrate that beta-D-galactosidase production in supernates of anaerobic cultures was significantly (P < 0.01) reduced in feces from patients with active Crohn's disease (N = 7), when compared to healthy controls (N = 8). Therefore using X-gal and selective media, we enumerated bacteria able to release beta-D-galactosidase in feces from patients with active (N = 16) or quiescent disease (N = 5) and healthy controls (N = 14). Bifidobacteria numbers were significantly reduced in patients (P < 0.01 for active; P < 0.02 for quiescent disease) whereas Bacteroides and Lactobacilli counts remained unchanged. beta-D-Galactosidase activity and Bifidobacteria counts were significantly correlated (P < 0.03). Bifidobacteria are regarded as beneficial for the host. The reduction in Bifidobacteria is responsible for decreased beta-D-galactosidase activity. Thus oral administration of prebiotics that promote their growth might have potential therapeutic interest.

Escherichia coli strains isolated from patients with Crohn's disease (CD) with chronic ileal lesions (n=14), early endoscopic recurrent lesions (n=20), without endoscopic recurrence (n=7), and controls (n=21) were compared by ribotyping. The dendrogram generated by 50 ribotype profile analysis revealed a large cluster of genetically linked E coli strains isolated significantly more frequently from patients with chronic and recurrent CD (24/33 patients) than from controls (9/21) (p<0.05). Most patients operated on for chronic ileal lesions (78.5%) harboured E coli strains belonging to cluster A (p<0.002 v controls). The prevalence of patients with early recurrent lesions harbouring E coli strains belonging to this cluster was high but not significant, although 16 strains isolated from eight patients presented the same ribotype profile. In this cluster, 21 of 26 strains isolated from patients with active CD demonstrated adherent ability to differentiated Caco-2 cells, indicating that most of the genetically related strains share a common virulence trait. Comparison of E coli strains recovered from ulcerated and healthy mucosa of patients operated on for CD demonstrated in each patient that a single strain colonised the intestinal mucosa. Our results suggest that although a single E coli isolate was not found in Crohn's ileal mucosa, some genotypes were more likely than others to be associated with chronic or early recurrent ileal lesions.