Commensal bacteria

Quigley, Eamonn Martin

doi:10.1097/mco.0b013e328348c033

Cited by 9 publications

(4 citation statements)

References 71 publications

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“…A study investigating IBS symptoms in IBD patients who were thought to be in clinical remission demonstrated high levels of calprotectin levels; this suggests that in most cases IBS symptoms are the result of undetected ongoing inflammation 164. Underlying mechanistic links are lacking but it is tempting to raise the hypothesis that the intestinal microbiota may be a common factor in both diseases 165. In fact, as with IBS (tables 2 and 3), faecal166–171 and mucosal-associated dysbiosis167 172–178 has been described IBD.…”

Section: Gi Disorders Mimicking and Overlapping With Fbdsmentioning

confidence: 99%

Intestinal microbiota in functional bowel disorders: a Rome foundation report

Simrén

Barbara

Flint

et al. 2012

Gut

784

658

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It is increasingly perceived that gut host–microbial interactions are important elements in the pathogenesis of functional gastrointestinal disorders (FGID). The most convincing evidence to date is the finding that functional dyspepsia and irritable bowel syndrome (IBS) may develop in predisposed individuals following a bout of infectious gastroenteritis. There has been a great deal of interest in the potential clinical and therapeutic implications of small intestinal bacterial overgrowth in IBS. However, this theory has generated much debate because the evidence is largely based on breath tests which have not been validated. The introduction of culture-independent molecular techniques provides a major advancement in our understanding of the microbial community in FGID. Results from 16S rRNA-based microbiota profiling approaches demonstrate both quantitative and qualitative changes of mucosal and faecal gut microbiota, particularly in IBS. Investigators are also starting to measure host–microbial interactions in IBS. The current working hypothesis is that abnormal microbiota activate mucosal innate immune responses which increase epithelial permeability, activate nociceptive sensory pathways and dysregulate the enteric nervous system. While we await important insights in this field, the microbiota is already a therapeutic target. Existing controlled trials of dietary manipulation, prebiotics, probiotics, synbiotics and non-absorbable antibiotics are promising, although most are limited by suboptimal design and small sample size. In this article, the authors provide a critical review of current hypotheses regarding the pathogenetic involvement of microbiota in FGID and evaluate the results of microbiota-directed interventions. The authors also provide clinical guidance on modulation of gut microbiota in IBS.

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Section: Gi Disorders Mimicking and Overlapping With Fbdsmentioning

confidence: 99%

Intestinal microbiota in functional bowel disorders: a Rome foundation report

Simrén

Barbara

Flint

et al. 2012

Gut

784

658

View full text Add to dashboard Cite

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“…Evidence from distant disciplines such as molecular biology, immunology and clinical research converges on abnormal interactions between the host and the external human microbiome in the pathogenesis of IBS [14] and IBD [22], establishing an etiological interface between IBS and IBD [23]. Molecular interaction between host cells and commensal enteric bacteria, or transient acute gastroenteritis induced by specific pathogens, could lead to a continuous activation of cells of the innate and acquired immune system causing chronically perceived symptoms or lasting injury to part of the GI tract.…”

Section: Discussionmentioning

confidence: 99%

“…Molecular interaction between host cells and commensal enteric bacteria, or transient acute gastroenteritis induced by specific pathogens, could lead to a continuous activation of cells of the innate and acquired immune system causing chronically perceived symptoms or lasting injury to part of the GI tract. The efficacy of antibiotic therapy in IBS and IBD provides some support for such a patho-mechanism [22,23], although theoretical interest in small intestinal bacterial overgrowth is decreasing [23]. However, our observation that FD and IBS symptomatology improve significantly during PPI treatment, although at a slower rate than the signs and symptoms of GERD [18], could possibly favour an underlying mechanism that is primarily immune-mediated rather than based on neural process.…”

Section: Discussionmentioning

confidence: 99%

Possible etiology of improvements in both quality of life and overlapping gastroesophageal reflux disease by proton pump inhibitor treatment in a prospective randomized controlled trial

et al. 2013

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BackgroundSymptoms suggestive of functional dyspepsia (FD) and irritable bowel syndrome (IBS) frequently overlap with those of gastroesophageal reflux disease. Despite the high prevalence of symptomatic overlap, the underlying etiology remains poorly defined. We assessed the correlation of symptomatic relief and health-related quality of life (HRQoL) with healing of reflux esophagitis to further derive insights into the underlying etiology.Methods626 patients with reflux esophagitis were enrolled into one of two treatment groups (classical healing concept or the complete remission concept) to investigate differences in treatment intensity. Patients were treated with pantoprazole until esophageal mucosal healing. Remission was followed for up to 6 months without treatment. Gastro-intestinal symptoms and HRQoL were analyzed using disease-specific, psychometrically validated patient-reported outcome instruments (ReQuest™, GERDyzer™).ResultsSymptomatic burden reflected by ReQuest™ substantially decreased from baseline to end of treatment by 83% and 88% in either treatment group, respectively. ReQuest™ scores significantly decreased in patients with or without heartburn and in those with symptoms suggestive of FD and IBS, indicating response of all symptom categories to treatment (p < 0.005). Therapy-associated relief of symptoms was paralleled by substantial gains in HRQoL, which continued to stabilize post-treatment.ConclusionsPantoprazole is effective in relieving upper and lower gastro-intestinal symptoms overlapping with erosive esophagitis, and provides sustained improvement in HRQoL post-treatment. Our results propose a link between both healing of erosive esophagitis and the slower remission of upper and lower gastro-intestinal symptoms. Since the improvement observed is likely to be multifactorial, the possibility for an immune-mediated etiology and identification of putative susceptibility factors by genome-wide association study may provide focus for future research.Trial registrationClinicalTrials.gov identifier: NCT00325676.

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“…Interestingly, abnormalities of the gut microbiota are present in common intestinal conditions, including irritable bowel syndrome, chronic idiopathic diarrhoea, and IBD[ 61 - 63 ]. In addition, recent evidence has suggested that the impact of the intestinal microbiota in disease pathogenesis can extend to other immune-mediated conditions beyond the gut including, for example, type 1 diabetes, cardiovascular disease, and autoimmune demyelination[ 64 - 66 ].…”

Section: Intestinal Microbiota-host Interactions and The Development mentioning

confidence: 99%

Diet and microbiota in inflammatory bowel disease: The gut in disharmony

Rapozo

Bernardazzi

Souza

2017

WJG

137

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Bacterial colonization of the gut shapes both the local and the systemic immune response and is implicated in the modulation of immunity in both healthy and disease states. Recently, quantitative and qualitative changes in the composition of the gut microbiota have been detected in Crohn’s disease and ulcerative colitis, reinforcing the hypothesis of dysbiosis as a relevant mechanism underlying inflammatory bowel disease (IBD) pathogenesis. Humans and microbes have co-existed and co-evolved for a long time in a mutually beneficial symbiotic association essential for maintaining homeostasis. However, the microbiome is dynamic, changing with age and in response to environmental modifications. Among such environmental factors, food and alimentary habits, progressively altered in modern societies, appear to be critical modulators of the microbiota, contributing to or co-participating in dysbiosis. In addition, food constituents such as micronutrients are important regulators of mucosal immunity, with direct or indirect effects on the gut microbiota. Moreover, food constituents have recently been shown to modulate epigenetic mechanisms, which can result in increased risk for the development and progression of IBD. Therefore, it is likely that a better understanding of the role of different food components in intestinal homeostasis and the resident microbiota will be essential for unravelling the complex molecular basis of the epigenetic, genetic and environment interactions underlying IBD pathogenesis as well as for offering dietary interventions with minimal side effects.

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Commensal bacteria

Cited by 9 publications

References 71 publications

Intestinal microbiota in functional bowel disorders: a Rome foundation report

Intestinal microbiota in functional bowel disorders: a Rome foundation report

Possible etiology of improvements in both quality of life and overlapping gastroesophageal reflux disease by proton pump inhibitor treatment in a prospective randomized controlled trial

Diet and microbiota in inflammatory bowel disease: The gut in disharmony

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