The new biopsychosocial model of disorders of gut–brain interaction

The understanding of disorders of gut–brain interaction (DGBI) has evolved substantially over the years, moving from a simplistic view of psychosomatic conditions occurring in the absence of organic disease to a more comprehensive biopsychosocial model linking gastrointestinal (GI) dysfunction to dysregulation of the gut–brain axis. In this view, stressors, such as life stresses, infection or inflammation, especially occurring in early postnatal life, can influence the psychosocial milieu of the individual, gut physiological state (motility, sensation, immune state, microbiota composition, reaction to nutrients), and their mutual interaction through the brain–gut axis. A critical component of this axis is the enteric nervous system (ENS), which controls moment-to-moment GI functions by integrating signals from multiple cell types within the gut wall and from the brain via autonomic nerves. Neurons and glia within the enteric neurocircuits regulate these functions, including epithelial fluid exchange, smooth muscle activity, and visceral sensitivity. Defects in ENS function driven by stressors are likely to play a central role in DGBI and often manifest as chronic, sexually dimorphic increases in visceral sensitivity, GI dysmotility, increases in gut permeability, or a combination of these. Importantly, alterations in ENS function can themselves contribute to persistent changes in gut–brain signaling and symptom generation.This Research Topic aims to deepen our understanding of how stressors influence the physiological functioning of the ENS, leading to persistent gut dysfunction and altered gut–brain signaling. We are particularly interested in mechanism-based research linking DGBI to stress and exploring epigenetic and environmental influences on gut function, including motility and visceral sensitivity, mucosal immune function and inflammation, gut microbiota, and responses to food and nutritional factors. Emphasis will be placed on studies showing how these effects are mediated through interactions between the ENS and other cell types within the gut, including enteroendocrine, interstitial, epithelial, immune, and smooth muscle cells, as well as the gut microbiota. Studies examining how dietary patterns, including Western diet exposure, influence the gut microbiome and, more broadly, gut physiology, immune function, and ENS plasticity are also encouraged. The goal is to bring together evidence to build a more comprehensive mechanistic understanding of stress-induced gut dysfunction while identifying underlying pathways and potential targets for therapeutic intervention for DGBI.We welcome Original Research, Review, Mini Review, and Perspective articles addressing:• Epigenetic regulation of ENS plasticity (e.g., gene expression, DNA methylation, histone modifications, chromatin remodeling, non-coding RNAs)• Early-life stressor-induced ENS plasticity (e.g., psychological stress, maternal separation, infection, inflammation, nutritional alterations)• Neuroimmune interactions and ENS plasticity (e.g., enteric glia–immune cell and neurons-immune cell signaling, cytokines, mast cells, macrophages, neuroinflammation)• Environmental factors and ENS plasticity (e.g., Western diet and other dietary patterns, nutrients, antibiotics, medications, environmental exposures, and their effects on the gut microbiome and gut physiology)• Microbiome–ENS interactions and plasticity (e.g., microbial metabolites, short-chain fatty acids, bile acids, tryptophan metabolites, dysbiosis, and diet–microbiome–ENS interactions)• Gut–brain and autonomic pathways in ENS plasticity (e.g., bidirectional gut–brain signaling, autonomic regulation, stress-induced alterations in enteric neural circuits, and mechanisms linking ENS dysfunction to persistent changes in gut–brain communication) Topic editors: Dmitrii Pavlov, Luisa Seguella Source: https://www.frontiersin.org/research-topics/82080/the-new-biopsychosocial-model-of-disorders-of-gut-brain-interaction