Exploring Different Effects of Exclusive Enteral Nutrition (EEN) and Corticosteroids on the Gut Microbiome in Crohn's Disease Based on a Three-Stage Strategy

Dong Guo, Liang Fang, Ruiqing Liu, Yu Li, Liang Lv, Zhaojiao Niu, Dong Chen, Yanbing Zhou, Weiming Zhu, Dong Guo, Liang Fang, Ruiqing Liu, Yu Li, Liang Lv, Zhaojiao Niu, Dong Chen, Yanbing Zhou, Weiming Zhu

Abstract

The objective of this study was to compare the efficacy of exclusive enteral nutrition (EEN) and corticosteroids on the gut microbiome in Crohn's disease. Methods. Data were collected for 16 patients newly diagnosed with CD as the test group and 10 healthy volunteers as the control group. The 16 patients were randomly divided into the EEN group and the corticosteroids group. For subsequent analysis, 6 patients in the EEN group with follow-up were enrolled to compare the 0-month, 1-month, and 3-month outcomes. We analyzed and compared gut microbiota between different groups in 3 stages. To evaluate the clinical outcome of treatment, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), hemoglobin (HB), albumin (ALB), and Crohn's disease activity (CDAI) were recorded. Results. There are significant differences in microbiota between patients with CD and healthy people, and there are intuitive differences in the main components of the microbiota. 16 patients were included in stage 2, in which both corticosteroids and EEN can induce CD remission well. However, corticosteroids have a greater impact on inflammatory indicators, while EEN has a more obvious effect on nutritional indicators. Principal component analysis suggests that there are different compositional changes in the gut microbiome after corticosteroids and EEN treatment. After 3 months of dynamic observation, we found that EEN can effectively maintain CD remission, reduce inflammatory indicators, and improve nutritional indicators. Conclusions. Both EEN and corticosteroids can increase the diversity of the microbiome in inducing CD remission, while they have different effects on the proportion of microbiome species. This trial is registered with NCT02056418.

Conflict of interest statement

The authors declare that they have no conflicts of interest.

Copyright © 2022 Dong Guo et al.

Figures

Figure 1
Figure 1
The flow chart of the three-stage research.
Figure 2
Figure 2
PCA in three stage. Abbreviations: HC: health control; CD: Crohn's Disease; GCPR: before corticosteroids treatment; ENPR: before EEN treatment; GCPO: after corticosteroids treatment; ENPO: after EEN treatment; EN0: 0 month after EEN treatment; EN1: 1 month after EEN treatment; EN3: 3 months after EEN treatment.
Figure 3
Figure 3
The number of OTU in different groups. Abbreviations: HC: health control; CD: Crohn's Disease; GCPR: before corticosteroids treatment; ENPR: before EEN treatment; GCPO: after corticosteroids treatment; ENPO: after EEN treatment; EN0: 0 month after EEN treatment; EN1: 1 month after EEN treatment; EN3: 3 months after EEN treatment.
Figure 4
Figure 4
Phyla measurement of the 3 stage. Abbreviations: EN0: 0 month after EEN treatment; EN1: 1 month after EEN treatment; EN3: 3 months after EEN treatment.

References

    1. Torres J., Mehandru S., Colombel J. F., Peyrin–Biroulet L. Crohn’s disease. The Lancet . 2017;389(10080):1741–1755.
    1. Veauthier B., Hornecker J. R. Crohn’s disease: diagnosis and management. American family physician . 2018;98(11):661–669.
    1. Mazal J., Truluck C. Organizing and leading a journal club. Radiologic technology . 2014;85(5):549–553.
    1. MacLellan A., Connors J., Grant S., Cahill L., Langille M., van Limbergen J. The impact of exclusive enteral nutrition (EEN) on the gut microbiome in Crohn’s disease: a review. Nutrients . 2017;9(5):p. 0447. doi: 10.3390/nu9050447.
    1. Ashton J. J., Gavin J., Beattie R. M. Exclusive enteral nutrition in Crohn’s disease: evidence and practicalities. Clinical nutrition . 2019;38(1):80–89. doi: 10.1016/j.clnu.2018.01.020.
    1. Svolos V., Hansen R., Nichols B., et al. Treatment of active Crohn’s disease with an ordinary food-based diet that replicates exclusive enteral nutrition. Gastroenterology . 2019;156(5):1354–1367.e6. doi: 10.1053/j.gastro.2018.12.002.
    1. Coward S., Kuenzig M. E., Hazlewood G., et al. Comparative effectiveness of mesalamine, sulfasalazine, corticosteroids, and budesonide for the induction of remission in Crohn’s disease: a Bayesian network metaanalysis. Inflammatory bowel diseases . 2017;23(3):461–472. doi: 10.1097/MIB.0000000000001023.
    1. Du J., Fu L., Sui Y., Zhang L. The function and regulation of OTU deubiquitinases. Frontiers of Medicine . 2020;14(5):542–563. doi: 10.1007/s11684-019-0734-4.
    1. Weingarden A. R., Vaughn B. A.-O. Intestinal microbiota, fecal microbiota transplantation, and inflammatory bowel disease. Gut microbes . 2017;8(3):238–252. doi: 10.1080/19490976.2017.1290757.
    1. Swidsinski A., Ladhoff A., Pernthaler A., et al. Mucosal flora in inflammatory bowel disease. Gastroenterology . 2002;122(1):44–54. doi: 10.1053/gast.2002.30294.
    1. Ungaro R., Bernstein C. N., Gearry R., et al. Antibiotics associated with increased risk of new-onset Crohn’s disease but not ulcerative colitis: a meta-analysis. The American journal of gastroenterology . 2014;109(11):1728–1738. doi: 10.1038/ajg.2014.246.
    1. Borrelli O., Cordischi L., Cirulli M., et al. Polymeric diet alone versus corticosteroids in the treatment of active pediatric Crohn’s disease: a randomized controlled open-label trial. Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association . 2006;4(6):744–753. doi: 10.1016/j.cgh.2006.03.010.
    1. Andoh A., Tsujikawa T., Sasaki M., et al. Faecal microbiota profile of Crohn’s disease determined by terminal restriction fragment length polymorphism analysis. Alimentary pharmacology & therapeutics . 2009;29(1):75–82. doi: 10.1111/j.1365-2036.2008.03860.x.
    1. Day A. S., Whitten K. E., Lemberg D. A., et al. Exclusive enteral feeding as primary therapy for Crohn’s disease in Australian children and adolescents: a feasible and effective approach. Journal of gastroenterology and hepatology . 2006;21(10):1609–1614. doi: 10.1111/j.1440-1746.2006.04294.x.
    1. Levin A. D., Wadhera V., Leach S. T., et al. Vitamin D deficiency in children with inflammatory bowel disease. Digestive diseases and sciences . 2011;56(3):830–836. doi: 10.1007/s10620-010-1544-3.
    1. Afzal N. A., Van der Zaag‐Loonen H. J., Arnaud‐Battandier F., et al. Improvement in quality of life of children with acute Crohn’s disease does not parallel mucosal healing after treatment with exclusive enteral nutrition. Alimentary pharmacology & therapeutics . 2004;20(2):167–172. doi: 10.1111/j.1365-2036.2004.02002.x.
    1. Guo Z., Wu R., Zhu W., et al. Effect of exclusive enteral nutrition on health-related quality of life for adults with active Crohn's disease. Nutrition in clinical practice: official publication of the American Society for Parenteral and Enteral Nutrition . 2013;28(4):499–505. doi: 10.1177/0884533613487218.
    1. Martin H. M., Campbell B. J., Hart C. A., et al. Enhanced _Escherichia coli_ adherence and invasion in Crohn’s disease and colon cancer. Gastroenterology . 2004;127(1):80–93. doi: 10.1053/j.gastro.2004.03.054.
    1. Dobashi K., Weiner D. B., Greene M. I. Differential regulation of oncogenic and cellular p185 by serine/threonine kinases. DNA . 1989;8(10):723–732. doi: 10.1089/dna.1989.8.723.
    1. Rolhion N., Darfeuille-Michaud A. Adherent-invasive Escherichia coli in inflammatory bowel disease. Inflammatory bowel diseases . 2007;13(10):1277–1283. doi: 10.1002/ibd.20176.

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