Abstract
The complex bidirectional communication system existing between the gastrointestinal tract and the brain initially termed the “gut–brain axis” and renamed the “microbiota–gut–brain axis”, considering the pivotal role of gut microbiota in sustaining local and systemic homeostasis, has a fundamental role in the pathogenesis of Inflammatory Bowel Disease (IBD). The integration of signals deriving from the host neuronal, immune, and endocrine systems with signals deriving from the microbiota may influence the development of the local inflammatory injury and impacts also more distal brain regions, underlying the psychophysiological vulnerability of IBD patients. Mood disorders and increased response to stress are frequently associated with IBD and may affect the disease recurrence and severity, thus requiring an appropriate therapeutic approach in addition to conventional anti-inflammatory treatments. This review highlights the more recent evidence suggesting that alterations of the microbiota–gut–brain bidirectional communication axis may concur to IBD pathogenesis and sustain the development of both local and CNS symptoms. The participation of the main microbial-derived metabolites, also defined as “postbiotics”, such as bile acids, short-chain fatty acids, and tryptophan metabolites in the development of IBD-associated gut and brain dysfunction will be discussed. The last section covers a critical evaluation of the main clinical evidence pointing to the microbiome-based therapeutic approaches for the treatment of IBD-related gastrointestinal and neuropsychiatric symptoms.
Highlights
Alterations of the microbial composition and load may concur to the development of local response to inflammation but may extend their influence to more distant sites through the gut–brain axis, giving rise to psychiatric manifestations, frequently reported in Inflammatory Bowel Disease (IBD) patients and negatively impacting on the patient’s mental status
A clear-cut demonstration of a causative relationship between dysbiosis and IBD has not been provided yet, in recent years, efforts in the field of metabolomics techniques in conjunction with observational and experimental data have highlighted the mechanistic contribution of microbial metabolites, defined as “postbiotics”, to the pathogenesis of IBD
We have shown that SCFAs, secondary bile acids, and TRP metabolites may have neural, immune, and endocrine control of inflammation, and of the mental health status during chronic intestinal inflammation
Summary
The gut microbiota is a fundamental player in gut–brain communication by releasing a plethora of metabolites, which are involved in the control of local metabolic, neuronal, and immune functions and extend their actions to more distal regions within the CNS, being critical for brain development and homeostasis [25,26,27] In this context, changes within the symbiotic interplay between the host and the saprophytic microflora during IBD may bear important consequences for the host health, underlying development of gastrointestinal symptoms and favoring the patient psychophysiological vulnerability [22,24,28]. Sci. 2021, 22, 1623 a critical evaluation of the main available clinical evidence pointing to the manipulation of the saprophytic gut microflora as a possible adjuvant approach for the treatment of IBD-related gastrointestinal and neuropsychiatric symptoms
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