scholarly journals The impact of exclusive enteral nutrition on the intestinal microbiota in inflammatory bowel disease

2018 ◽  
Vol 4 (4) ◽  
pp. 584-593 ◽  
Author(s):  
Andrew S Day ◽  
2015 ◽  
Author(s):  
Lindsey Albenberg ◽  
Robert Baldassano

Enteral nutrition therapy is a dietary treatment regimen for inflammatory bowel disease that has the benefit of avoiding suppression of the immune system. Its mechanism of action has not been well characterized, but may be related to the elimination of dietary antigens or modulation of the gut microbiota. This treatment has shown success for induction of remission, and may also have a role in maintenance of remission. In the pediatric population, enteral nutrition therapy has the dual benefit of targeting both the inflammatory processes and the poor growth of these patients. This review details the administration and mechanism of action of enteral nutritional therapy, the induction and maintenance of remission, the impact of enteral nutritional therapy on growth and nutrition, and side effects and quality of life. A table summarizes studies investigating enteral nutritional therapy for induction of remission. This review contains 1 table and 49 references.


Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 414 ◽  
Author(s):  
Helena Rolandsdotter ◽  
Kerstin Jönsson-Videsäter ◽  
Ulrika L. Fagerberg ◽  
Yigael Finkel ◽  
Michael Eberhardson

Exclusive Enteral Nutrition (EEN) is the first-line treatment in children with Crohn’s disease (CD) for induction of remission. However, the mode of action remains conjectural. The aim of this study was to investigate whether the effect of EEN is paralleled by changes in the mucosal cytokine profiles (MCP). Twelve children with new onset inflammatory bowel disease (IBD) received induction treatment with a polymeric EEN. We assessed clinical, endoscopic and histologic scoring before and after EEN. Twelve colonic cytokines were analyzed by Polymerase Chain Reaction (PCR) in six of the IBD patients at onset and after EEN as well as in six non-IBD control children at the diagnostic colonoscopy. Twelve children completed 6 weeks of EEN, except from one child who completed 4 weeks. At the control colonoscopy, 83% were in complete clinical remission. Changes were found in the MCPs of individual patients after EEN. In particular, children with IBD showed significantly higher values of Interleukin (IL)-12β (p = 0.008) and IL-23α (p = 0.02) compared to non-IBD controls at the diagnostic colonoscopy. Furthermore, an overall change in proinflammatory cytokines was noted in the IBD-group after treatment. Further studies are warranted to understand the role of EEN in MCP.


2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S010-S011
Author(s):  
E Brand ◽  
Y Laenen ◽  
F van Wijk ◽  
M de Zoete ◽  
B Oldenburg

Abstract Background The pathogenesis of inflammatory bowel disease (IBD) is thought to result from an interplay between microbiota, the immune system and the environment in genetically susceptible hosts. Immunoglobulin A (IgA) produced by the immune system can be specifically directed against bacteria. The IgA-coating pattern of intestinal bacteria thus reflects interactions between the immune system and specific bacteria. Studying IBD in twins, concordant and discordant for IBD, reduces the impact of genetic predisposition and childhood exposures and therefore offers the unique opportunity to focus on other factors such as intestinal microbiota composition and immune-interactions in IBD. Methods Faecal samples from twin pairs discordant for Crohn’s disease (CD) or ulcerative colitis (UC) were collected. Employing fluorescence-activated cell sorting, IgA+ and IgA− bacteria from the intestinal microbiota were sorted. Subsequently, (1) the total, (2) IgA+ and (3) IgA− microbial composition was determined by 16S rRNA sequencing (IgA-SEQ). We estimated the relative IgA coating per bacterial species by dividing the abundance of that species in the IgA+ fraction over the abundance in the IgA- fraction, representing the IgA coating index. Linear discriminant analyses were performed with LefSE. Results We included 31 twin pairs (62 individuals) discordant for IBD (CD: 15, UC: 16). 15/32 twin pairs were monozygotic, 43/62 of participants were female, the median age was 47 years (interquartile range: 34–58.5). Of 31 participants with IBD, 7 had signs of active inflammation based on endoscopy, Harvey–Bradshaw index or short clinical colitis activity index. Differences (log-linear discriminant analysis score >3) in the microbial composition of IgA-coated bacteria were observed between CD patients and their twin-siblings not affected by IBD: Dorea formicigenerans (increased in IgA coating), Parabacteroides sp., Christensenellaceae sp., Clostridium sp. and Mollicutes RF39 sp. (decreased in IgA coating). In ulcerative colitis patients, an increase in IgA-coating was observed for Ruminococcus gnavus and Dorea formicigenerans, while Turicibacter sp., Barnesiellaceae sp. and an unclassified Clostridiales sp. were decreased in IgA-coating compared with their twin-siblings not affected by IBD. Conclusion In twins affected by IBD, the pattern of IgA-coated bacteria differs between IBD and non-IBD affected individuals. These data on immune-bacteria interactions could serve as a starting point for the elucidation of the immune-responses triggered by specific bacteria in IBD.


Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 808
Author(s):  
Aïcha Zouggar ◽  
Joshua R. Haebe ◽  
Yannick D. Benoit

In a recent publication, Ansari et al. identified gut microbiota as a critical mediator of the intestinal inflammatory response through epigenetic programming of host intestinal epithelium. Exposure to the microbiota induces Ten-Eleven-Translocation (TET)-dependent hypomethylation of genomic elements regulating genes associated with inflammatory response and colorectal cancer. Here, we discuss the impact of such a discovery on the understanding of how the intestinal microbiota may contribute to epigenetic reprogramming and influence the onset of colorectal tumorigenesis. Finally, we examine the prospect of TET inhibition strategies as a therapeutic and/or preventive approach for colorectal cancer in patients afflicted by inflammatory bowel disease.


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