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Copyright ©The Author(s) 2016.
World J Gastroenterol. Feb 21, 2016; 22(7): 2219-2241
Published online Feb 21, 2016. doi: 10.3748/wjg.v22.i7.2219
Figure 1
Figure 1 Gut microbiota influences the bidirectional communication between the enteric nervous system and the central nervous system, modulating gut development and several physiological functions, including intestinal motility, sensitivity, secretion and immunity. In irritable bowel syndrome (IBS), the altered composition and/or activity of microbiota may induce a disruption of this communication leading to activation of immune system and production of pro-inflammatory cytokines, production of microbial metabolites as short-chain fatty acids (SCFAs) that are toxic at high concentration, activation of hypothalamic-pituitary-adrenal (HPA) axis with increase of cortisol that feeds back to the pituitary, hypothalamus (HYP), amygdala (AMG), hippocampus (HIPP) and prefrontal cortex to shut off the HPA axis and increase of corticotropin releasing factor (CRF). These effects lead to alterations of intestinal motility and sensation, disruption of epithelial barrier and impaired production of neurotransmitters with an increased response to stressful events. On turn, stress may provoke systemic pro-inflammatory cytokines production that activates the HPA axis that signals to both enteric nervous system and the central nervous system and may alter microbiota composition.