Microbiota in the etiopathogenesis and treatment of the symptomatic diverticular disease of the large bowel

Česká verzia

Authors: Gombošová L.
Authors place of work: I. interná klinika LF UPJŠ a UNLP, Košice
Published in the journal: Gastroent Hepatol 2019; 73(5): 418-422
Category: Clinical and Experimental Gastroenterology: Review Article
doi: https://doi.org/10.14735/amgh2019418

Summary

Pathological changes in microbiota play a key role in the etiopathogenesis of symptomatic diverticular disease (DD) of the large bowel, as well as in immune dysregulation and visceral hypersensitivity. The large bowel is a diverse ecosystem whose two dominant microbiota are members of the phyla Firmicutes and Bacteroidetes, as well as viruses and fungi. Firmicutes represent 60–80% of the bacteria of the large bowel; there are gram positive anaerobes and aerobes, some of which are spore forming, together with Faecalibacterium sp, Clostridium sp, Lactobacillacae, Biffidobacteria sp. Other than bacteria, the large bowel also contains fungi (referred to as mycobioma or fungoma) with massive representation of Candida sp. in adults. The types of fungi differ with age, environment, and stress. Large bowel microbiota are affected by many internal and external factors, such as stress, diseases, drugs, environment, and others. Metabolomic studies have shown that specific changes in microbiota characterize symptomatic DD. The management of symptomatic DD includes cyclic therapy with rifaximin, aimed at modulating gut microbiota and improving the symptom score of the disease.

Keywords:

dysbiosis – rifaximin – microbiota – symptomatic uncomplicated diverticular disease

Zdroje

1. Barbara G, Scaioli E, Barbaro MR et al. Gut microbiota, metabolome and immune signatures in patients with uncomplicated diverticular disease. Gut 2017; 66 (7): 1252–1261. doi: 10.1136/gutjnl-2016-312377.

2. Mearin F, Gasbarrini A, Malfertheiner P et al. Gut microbiota: modulate its complexity to restore the balance. EMJ Gastroenterol 2015; 4 (1): 66–71.

3. Hills RD Jr, Pontefract BA, Mishcon HR et al. Gut microbiome: profound implications for diet and disease. Nutrients 2019; 11 (7): pii: E1613. doi: 10.3390/nu11071613.

4. Tursi A. Current and evolving concepts on the pathogenesis of diverticular disease. J Gastrointestin Liver Dis 2019; 28: 225–235. doi: 10.15403/jgld-184.

5. Valdes MA, Walter J, Segal E et al. Role of the gut microbiota in nutrition and health. BMJ 2018; 361: k2179. doi: 10.1136/bmj.k2179.

6. Jandhyala SM, Talukdar R, Subramanyam C et al. Role of the normal gut microbiota. World J Gastroenterol 2015; 21 (29): 8787–8803. doi: 10.3748/wjg.v21.i29.8787.

7. Linninge C, Roth B, Erlanson-Albertsson C et al. Abundance of Enterobacteriaceae in the colon mucosa in diverticular disease. World J Gastrointest Pathophysiol 2018; 9 (1): 18–27. doi: 10.4291/wjgp.v9.i1.18.

8. Lopetuso LR, Petito V, Graziani C et al. Gut microbiota in health, diverticular disease, irritable bowel syndrome, and inflammatory bowel diseases: time for microbial marker of gastrointestinal disorders. Dig Dis 2018; 36 (1): 56–65. doi: 10.1159/000477205.

9. Spiller RC, Sloan TJ. Do diverticula provide a unique niche for microbiota which can lead to activation of the innate immune system? Gut 2017; 66 (7): 1175–1176. doi: 10.1136/gutjnl-2016-312928.

10. Bischoff SC, Barbara G, Buurman W et al. Intestinal permeability – a new target for disease prevention and therapy. BMC Gastroenterol 2014; 14: 189. doi: 10.1186/s12876-014-01 89-7.

11. Augustyn M, Grys I, Kukla M. Small intestinal bacterial overgrowth and nonalcoholic fatty liver disease. Clin Exp Hepatol 2019; 5 (1): 1–10. doi: 10.5114/ceh.2019.83151.

12. Carding S, Verbeke K, Vipond DT et al. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis 2015; 26: 26191. doi: 10.3402/mehd.v26.26191.

13. Bajaj JS, Barbara G, DuPont HL et al. New concepts on intestinal microbiota and the role of the non-absorbable antibiotics with special reference to rifaximin in digestive diseases. Dig Liv Dis 2018; 50 (8): 741–749. doi: 10.1016/j.dld.2018.04.020.

14. Tursi A, Mastromarino P, Capobianco D et al. Assessment of fecal microbiota and fecal metabolome in symptomatic uncomplicated diverticular disease of the dolon. J Clin Gastroenterol 2016; 50 (Suppl 1): S9–S12. doi: 10.1097/MCG.0000000000000626.

15. Laghi L, Mastromarino P, Elisei W et al. Impact of treatments on fecal microbiota and fecal metabolome in symptomatic uncomplicated diverticular disease of the colon: a pilot study. J Biol Regul Homeost Agents 2018; 32 (5): 1421–1432.

16. Turco F, Andreozzi P, Palumbo I et al. Bacterial stimuli activate nitric oxide colonic mucosal production in diverticular disease. Protective effects of L. casei DG® (Lactobacillus paracasei CNCM I-1572). United European Gastroenterol J 2017; 5 (5): 715–724. doi: 10.1177/2050640616684398.

17. Kvasnovsky CL, Leong LEX, Choo JM et al. Clinical and symptom scores are significantly correlated with fecal microbiota features in patients with symptomatic uncomplicated diverticular disease: a pilot study. Eur J Gastroenterol Hepatol 2018; 30 (1): 107–112. doi: 10.1097/MEG. 0000000000000995.

18. Carabotti M, Annibale B. Treatment of diverticular disease: an update on latest evidence and clinical implications. Drug Context 2018; 7: 212526. doi: 10.7573/dic.212526.

19. Ponziani FR, Zocco MA, D’Aversa F et al. Eubiotic properties of rifaximin: disruption of the traditional concepts in gut microbiota modulation. World J Gastroenterol 2017; 23 (25): 4491–4499. doi: 10.3748/wjg.v23.i25. 4491.

20. Ponziani FR, Scaldaferri F, Petito V et al. The role of antibiotics in gut microbiota modulation: the eubiotic effects of rifaximin. Dig Dis 2016; 34 (3): 269–278. doi: 10.1159/000443 361.