Autonomic nervous system as a key modulator in stress-related inflammatory bowel disease: Mechanisms and therapeutic implications

Figure 4 Stress-induced enteric nervous system signaling regulating intestinal immune responses. Stress activates the hypothalamic-pituitary-adrenal axis and autonomic nervous system, which modulate enteric nervous system activity and neuropeptide release. Enteric nervous system-derived substance P, vasoactive intestinal peptide, and neuropeptide Y regulate immune cell activation, mast cell responses, group 3 innate lymphoid cells-mediated mucosal protection, and inflammatory signaling in mesenteric adipocytes. These neuroimmune interactions establish a bidirectional feedback loop that influences intestinal inflammation and disease progression. HPA: Hypothalamic-pituitary-adrenal axis; CRH: Corticotropin-releasing hormone; ANS: Autonomic nervous system; ENS: Enteric nervous system; MC: Mast cell; VIP: Vasoactive intestinal peptide; NPY: Neuropeptide Y; ILC3: Group 3 innate lymphoid cells; TNF-α: Tumor necrosis factor-α; SP: Substance P; IL: Interleukin. The pattern was created with BioGDP.com[14].