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Review
. 2020 Mar 26;8(6):1013-1025.
doi: 10.12998/wjcc.v8.i6.1013.

Microbiota-gut-brain axis and its affect inflammatory bowel disease: Pathophysiological concepts and insights for clinicians

Affiliations
Review

Microbiota-gut-brain axis and its affect inflammatory bowel disease: Pathophysiological concepts and insights for clinicians

Emanuele Sinagra et al. World J Clin Cases. .

Abstract

Despite the bi-directional interaction between gut microbiota and the brain not being fully understood, there is increasing evidence arising from animal and human studies that show how this intricate relationship may facilitate inflammatory bowel disease (IBD) pathogenesis, with consequent important implications on the possibility to improve the clinical outcomes of the diseases themselves, by acting on the different components of this system, mainly by modifying the microbiota. With the emergence of precision medicine, strategies in which patients with IBD might be categorized other than for standard gut symptom complexes could offer the opportunity to tailor therapies to individual patients. The aim of this narrative review is to elaborate on the concept of the gut-brain-microbiota axis and its clinical significance regarding IBD on the basis of recent scientific literature, and finally to focus on pharmacological therapies that could allow us to favorably modify the function of this complex system.

Keywords: Gut-brain axis; Inflammatory bowel disease; Irritable bowel syndrome; Therapy.

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Conflict of interest statement

Conflict-of-interest statement: All the authors declare that this research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors, and thus there is no conflict of interest regarding this paper.

Figures

Figure 1
Figure 1
The main actors in the gut–brain-microbiota axis. The gut-brain-microbiota axis is defined as a two-way communication system that allows intestinal microbes to communicate with the brain and vice versa. The multiple inter-related structural networks of the central nervous system regulates autonomic nervous system input that alter gut microbial composition and function indirectly by modulating the microbial environment in the gut, and by affecting also the immune response. On the other hand, the gut microbiota can interact with the brain indirectly via gut-derived metabolites by acting on afferent vagal and/or spinal nerve endings, or directly via microbe-generated signals which act on enteroendocrine cells. Furthermore, the neuroendocrine signaling network mediated by the hypothalamic-pituitary-adrenal) axis, which is activated by the integrative reactions of specific centers in the central nervous system, represents a central integrative system mandatory for the successful physiological adaptation of our organism to different stressors.

References

    1. Schmidt C. Mental health: thinking from the gut. Nature. 2015;518:S12–S15. - PubMed
    1. Smith PA. The tantalizing links between gut microbes and the brain. Nature. 2015;526:312–314. - PubMed
    1. Mayer EA, Knight R, Mazmanian SK, Cryan JF, Tillisch K. Gut microbes and the brain: paradigm shift in neuroscience. J Neurosci. 2014;34:15490–15496. - PMC - PubMed
    1. Wang HX, Wang YP. Gut Microbiota-brain Axis. Chin Med J (Engl) 2016;129:2373–2380. - PMC - PubMed
    1. Simrén M, Barbara G, Flint HJ, Spiegel BM, Spiller RC, Vanner S, Verdu EF, Whorwell PJ, Zoetendal EG Rome Foundation Committee. Intestinal microbiota in functional bowel disorders: a Rome foundation report. Gut. 2013;62:159–176. - PMC - PubMed