Carroll IM, Ringel-Kulka T, Keku TO, Chang YH, Packey CD, Sartor RB et al.. Molecular analysis of the luminal- and mucosal-associated intestinal microbiota in diarrhea-predominant irritable bowel syndrome. Am J Physiol Gastrointest Liver Physiol 301: G799-G807

Division of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, 27599-7080, USA.
AJP Gastrointestinal and Liver Physiology (Impact Factor: 3.8). 07/2011; 301(5):G799-807. DOI: 10.1152/ajpgi.00154.2011
Source: PubMed


Alterations in the intestinal microbiota have been suggested as an etiological factor in the pathogenesis of irritable bowel syndrome (IBS). This study used a molecular fingerprinting technique to compare the composition and biodiversity of the microbiota within fecal and mucosal niches between patients with diarrhea-predominant IBS (D-IBS) and healthy controls. Terminal-restriction fragment (T-RF) length polymorphism (T-RFLP) fingerprinting of the bacterial 16S rRNA gene was used to perform microbial community composition analyses on fecal and mucosal samples from patients with D-IBS (n = 16) and healthy controls (n = 21). Molecular fingerprinting of the microbiota from fecal and colonic mucosal samples revealed differences in the contribution of T-RFs to the microbiota between D-IBS patients and healthy controls. Further analysis revealed a significantly lower (1.2-fold) biodiversity of microbes within fecal samples from D-IBS patients than healthy controls (P = 0.008). No difference in biodiversity in mucosal samples was detected between D-IBS patients and healthy controls. Multivariate analysis of T-RFLP profiles demonstrated distinct microbial communities between luminal and mucosal niches in all samples. Our findings of compositional differences in the luminal- and mucosal-associated microbiota between D-IBS patients and healthy controls and diminished microbial biodiversity in D-IBS fecal samples further support the hypothesis that alterations in the intestinal microbiota may have an etiological role in the pathogenesis of D-IBS and suggest that luminal and mucosal niches need to be investigated.

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    • "Development of fecal microbiota in young children J Cheng et al 2 The ISME Journal DNA was isolated from feces by modified protocol of the DNA clean-up Kit (Qiagen DNeasy Blood and Tissue extraction kit, Qiagen, Valencia, CA, USA), with mechanical disruption of bacterial cells followed by chemical extraction of DNA as previously described (Carroll et al., 2011). The concentration of isolated DNA was determined by using a Nanodrop spectrophotometer (Thermo Scientific, Asheville, NC, USA) before phylogenetic microarray analysis. "
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    ABSTRACT: The colonization pattern of intestinal microbiota during childhood may impact health later in life, but children older than 1 year are poorly studied. We followed healthy children aged 1-4 years (n=28) for up to 12 months, during which a synbiotic intervention and occasional antibiotics intake occurred, and compared them with adults from the same region. Microbiota was quantified with the HITChip phylogenetic microarray and analyzed with linear mixed effects model and other statistical approaches. Synbiotic administration increased the stability of Actinobacteria and antibiotics decreased Clostridium cluster XIVa abundance. Bacterial diversity did not increase in 1- to 5-year-old children and remained significantly lower than in adults. Actinobacteria, Bacilli and Clostridium cluster IV retained child-like abundances, whereas some other groups were converting to adult-like profiles. Microbiota stability increased, with Bacteroidetes being the main contributor. The common core of microbiota in children increased with age from 18 to 25 highly abundant genus-level taxa, including several butyrate-producing organisms, and developed toward an adult-like composition. In conclusion, intestinal microbiota is not established before 5 years of age and diversity, core microbiota and different taxa are still developing toward adult-type configuration. Discordant development patterns of bacterial phyla may reflect physiological development steps in children.The ISME Journal advance online publication, 2 October 2015; doi:10.1038/ismej.2015.177.
    The ISME Journal 10/2015; DOI:10.1038/ismej.2015.177 · 9.30 Impact Factor
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    • "In fact, the zebrafish has shown several unique advantages that make it superior to other animal model organisms for microbial investigation. To start with, the composition of the mucosal- and luminal-associated/faecal microbiota has been shown to be significantly different in human digestive tract [31,32]. Some believe the mucosal-associated microbiota seems of a closer link to the disease process than the faecal microbiota, as IBD is a disorder of mucosal inflammation. "
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    ABSTRACT: Inflammatory bowel disease (IBD) involves a breakdown in interactions between the host immune response and the resident commensal microbiota. Recent studies have suggested gut physiology and pathology relevant to human IBD can be rapidly modeled in zebrafish larvae. The aim of this study was to investigate the dysbiosis of intestinal microbiota in zebrafish models with IBD-like enterocolitis using culture-independent techniques. IBD-like enterocolitis was induced by exposing larval zebrafish to trinitrobenzenesulfonic acid (TNBS). Pathology was assessed by histology and immunofluorescence. Changes in intestinal microbiota were evaluated by denaturing gradient gel electrophoresis (DGGE) and the predominant bacterial composition was determined with DNA sequencing and BLAST and confirmed by real-time polymerase chain reaction. Larval zebrafish exposed to TNBS displayed intestinal-fold architecture disruption and inflammation reminiscent of human IBD. In this study, we defined a reduced biodiversity of gut bacterial community in TNBS-induced coliitis. The intestinal microbiota dysbiosis in zebrafish larvae with IBD-like colitis was characterized by an increased proportion of Proteobacteria (especially Burkholderia) and a decreased of Firmicutes(Lactobacillus group), which were significantly correlated with enterocolitis severity(Pearson correlation p < 0.01). This is the first description of intestinal microbiota dysbiosis in zebrafish IBD-like models, and these changes correlate with TNBS-induced enterocolitis. Prevention or reversal of this dysbiosis may be a viable option for reducing the incidence and severity of human IBD.
    BMC Microbiology 12/2013; 13(1):289. DOI:10.1186/1471-2180-13-289 · 2.73 Impact Factor
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    • "However Rajilic- Stojanovic et al recently showed that the fecal microbiota of IBS patients differs significantly from that of controls [117]. Only a handful of studies determined the mucosal microbiota in IBS patients [118] [119] [120] [121] [122], because the mucosal microbiota differs from the faecal microbiota and is in close contact proximity to the host its effect could be disproportional compared to the luminal bacteria. Unfortunately , none of the studies showed a significant effect, comparing IBS patients and healthy controls (Table 1). "
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    ABSTRACT: The human gastrointestinal tract is colonised with a dense and diverse microbial community, that is an important player in human health and physiology. Close to the epithelial cells the mucosal microbiota is separated from the host with a thin lining of host derived glycans, including the cell surface glycocalyx and the extracellular secreted mucus. The mucosa-associated microbial composition differs from the luminal content and could be particularly important for nutrient exchange, communication with the host, development of the immune system, and resistance against invading pathogens. The mucosa-associated microbiota has adapted to the glycan rich environment by the production of mucus-degrading enzymes and mucus-binding extracellular proteins, and include mucus-degrading specialists such as Akkermansia muciniphila and Bacteroides thetaiotaomicron. This review is focussed on the host-microbe interactions within the glycan landscape at the epithelial interface and considers the spatial organisation and composition of the mucosa-associated microbiota in health and disease.
    Best practice & research. Clinical gastroenterology 02/2013; 27(1):25-38. DOI:10.1016/j.bpg.2013.03.001 · 3.48 Impact Factor
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