Specific members of the predominant gut microbiota predict pouchitis following colectomy and IPAA in UC

Machiels, Kathleen; Sabino, João; Vandermosten, Leen; Joossens, Marie; Arijs, Ingrid; Bruyn, Magali de; Eeckhaut, Venessa; Assche, Gert Van; Ferrante, Marc; Verhaegen, Jan; Steen, Kristel Van; Immerseel, Filip Van; Huys, Geert; Verbeke, Kristin; Wolthuis, Albert; Overstraeten, Anthony de Buck van; D’Hoore, André; Rutgeerts, Paul; Vermeire, Séverine

doi:10.1136/gutjnl-2015-309398

Cited by 128 publications

(85 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Concurrent treatment of conventional guinea pigs with carrageenan and metronidazole, an antimicrobial primarily active against anaerobic bacteria, has been shown to prevent the development of intestinal ulcerations (22, 23). Consistent with recent reports in human IBD (24, 25), microorganisms such as Bacteroide s vulgatus appear to play an important role in the development of the experimental ulcerative lesions in animals (26). For example, animals who were immunized with B. vulgatus , prior to carrageenan administration developed experimental disease at a faster rate and more severe lesions than animals that were administered carrageenan alone (23, 27).…”

Section: The Role Of Carrageenan In Intestinal Inflammation In Animalsupporting

confidence: 89%

The Role of Carrageenan and Carboxymethylcellulose in the Development of Intestinal Inflammation

2017

View full text Add to dashboard Cite

Although the exact pathophysiology remains unknown, the development of inflammatory bowel disease (IBD) is influenced by the interplay between genetics, the immune system, and environmental factors such as diet. The commonly used food additives, carrageenan and carboxymethylcellulose (CMC), are used to develop intestinal inflammation in animal models. These food additives are excluded from current dietary approaches to induce disease remission in Crohn’s disease such as exclusive enteral nutrition (EEN) using a polymeric formula. By reviewing the existing scientific literature, this review aims to discuss the role that carrageenan and CMC may play in the development of IBD. Animal studies consistently report that carrageenan and CMC induce histopathological features that are typical of IBD while altering the microbiome, disrupting the intestinal epithelial barrier, inhibiting proteins that provide protection against microorganisms, and stimulating the elaboration of pro-inflammatory cytokines. Similar trials directly assessing the influence of carrageenan and CMC in humans are of course unethical to conduct, but recent studies of human epithelial cells and the human microbiome support the findings from animal studies. Carrageenan and CMC may trigger or magnify an inflammatory response in the human intestine but are unlikely to be identified as the sole environmental factor involved in the development of IBD or in disease recurrence after treatment. However, the widespread use of carrageenan and CMC in foods consumed by the pediatric population in a “Western” diet is on the rise alongside a corresponding increase in IBD incidence, and questions are being raised about the safety of frequent usage of these food additives. Therefore, further research is warranted to elucidate the role of carrageenan and CMC in intestinal inflammation, which may help identify novel nutritional strategies that hinder the development of the disease or prevent disease relapse post-EEN treatment.

show abstract

Section: The Role Of Carrageenan In Intestinal Inflammation In Animalsupporting

confidence: 89%

The Role of Carrageenan and Carboxymethylcellulose in the Development of Intestinal Inflammation

2017

View full text Add to dashboard Cite

show abstract

“…We showed a decrease in bacterial diversity and reduced abundance of predominant bacteria in UC pouches. R. gnavus infection, especially occurring as the predominant microbiota before colectomy, was shown to increase the risk of pouchitis 1 year after IPAA[12]. R. gnavus produces the bacteriocin ruminococcin A, which inhibits the growth of phylogenetically-related species and various bifidobacterial and clostridial species[32].…”

Section: Discussionmentioning

confidence: 99%

“…The findings of the most recent study revealed that disorders caused by protective and harmful bacteria are associated with pouch inflammation[11]. The emergence of Ruminococcus gnavus (R. gnavus ), Bacteriodes vulgatus and Clostridium perfringens (C. perfringens ) and deficiency of Blautia and Roseburia in patients with UC before IPAA is closely related to pouchitis[12]. …”

Section: Introductionmentioning

confidence: 99%

Fecal microbiota in pouchitis and ulcerative colitis

Wang

Wei

et al. 2016

WJG

View full text Add to dashboard Cite

AIMTo investigate the changes in microbiota in feces of patients with ulcerative colitis (UC) and pouchitis using genomic technology.METHODSFecal samples were obtained from UC patients with or without an ileal pouch-anal anastomosis (IPAA) procedure, as well as healthy controls. The touchdown polymerase chain reaction technique was used to amplify the whole V3 region of the 16S rRNA gene, which was transcribed from DNA extracted from fecal samples. Denaturing gradient gel electrophoresis was used to separate the amplicons. The band profiles and similarity indices were analyzed digitally. The predominant microbiota in different groups was confirmed by sequencing the 16S rRNA gene.RESULTSMicrobial biodiversity in the healthy controls was significantly higher compared with the UC groups (P < 0.001) and IPAA groups (P < 0.001). Compared with healthy controls, the UC patients in remission and those in the mildly active stage, the predominant species in patients with moderately and severely active UC changed obviously. In addition, the proportion of the dominant microbiota, which was negatively correlated with the disease activity of UC (r = -6.591, P < 0.01), was decreased in pouchitis patients. The numbers of two types of bacteria, Faecalibacterium prausnitzii and Eubacterium rectale, were reduced in UC. Patients with pouchitis had an altered microbiota composition compared with UC patients. The microbiota from pouchitis patients was less diverse than that from severely active UC patients. Sequencing results showed that similar microbiota, such as Clostridium perfringens, were shared in both UC and pouchitis.CONCLUSIONLess diverse fecal microbiota was present in patients with UC and pouchitis. Increased C. perfringens in feces suggest its role in the exacerbation of UC and pouchitis.

show abstract

“…Fecal microbiota transplantation (FMT) is an established therapeutic option for patients with recurrent Clostridioides difficile infection, and is also a promising therapeutic modality for patients with active UC with the aim of re-establishing the homeostasis of the intestinal microbiome [5, 6]. Microbial dysbiosis, which can only be controlled with antibiotics, is thought to be a major driver of clinical symptoms in patients with ADP [7]. A preliminary pilot study recently reported a sustained response for at least 3 months in 3 out of 5 ADP patients after FMT [8].…”

Section: Introductionmentioning

confidence: 99%

Combined Endoscopic and Oral Fecal Microbiota Transplantation in Patients with Antibiotic-Dependent Pouchitis: Low Clinical Efficacy due to Low Donor Microbial Engraftment

et al. 2019

View full text Add to dashboard Cite

Background and Objective: A significant number of pouch patients develop antibiotic-dependent pouchitis (ADP). Microbial dysbiosis is thought to be a major driver of clinical symptoms in ADP. The objective of this proof of concept study was to evaluate safety, efficacy, and donor microbial engraftment of an intensified fecal microbiota transplant (FMT) consisting of a single endoscopic FMT followed by daily oral FMT for 2 weeks in patients with ADP. Methods: We performed a prospective placebo-controlled double-blind FMT trial in patents with established ADP and planned to enroll 20 patients in this proof of concept study. In case of non-response, patients were offered an optional open label active FMT treatment. The endpoints were safety, clinical remission without need for antibiotics during 16 weeks of follow-up, quantitative changes of fecal calprotectin (FCP), and engraftment of donor FMT as determined by metagenomic sequencing of the V4 region of the 16S rRNA gene. Results: Due to a lower than expected clinical remission rate and low FMT engraftment, enrollment in the study was stopped prematurely after 6 patients were included. All 6 patients enrolled in the placebo-controlled portion failed to respond and needed antibiotic rescue therapy shortly after FMT. FCP increased in the majority of patients in the setting of relapse after FMT. In the active open label FMT extension study 1 out of 5 patients achieved antibiotic-free clinical remission. FMT engraftment after active FMT was observed only in this single patient, whereas engraftment of donor FMT occurred in none of the other patients receiving active FMT, paralleling the lack of clinical response. Conclusions: Low donor FMT engraftment resulted in low clinical efficacy of FMT in patients with ADP. Before embarking on larger clinical trials with FMT in patients with ADP or other forms of pouchitis, it is mandatory to explore approaches for superior FMT engraftment.

show abstract

Specific members of the predominant gut microbiota predict pouchitis following colectomy and IPAA in UC

Cited by 128 publications

References 67 publications

The Role of Carrageenan and Carboxymethylcellulose in the Development of Intestinal Inflammation

The Role of Carrageenan and Carboxymethylcellulose in the Development of Intestinal Inflammation

Fecal microbiota in pouchitis and ulcerative colitis

Combined Endoscopic and Oral Fecal Microbiota Transplantation in Patients with Antibiotic-Dependent Pouchitis: Low Clinical Efficacy due to Low Donor Microbial Engraftment

Contact Info

Product

Resources

About