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Abstract: The Gut-Brain Axis (GBA) is a complex, bidirectional communication network where persistent low-grade inflammation is central to the pathogenesis of numerous disorders, including Inflammatory Bowel Disease (IBD) and mood disorders. The Vagus Nerve (CN X) stands as the principal neural interface within this axis, dynamically regulating the host's inflammatory set-point. This review elucidates the Vagus Nerve's dual function as both an acute sensor of microbial and inflammatory signals (via approximately 80% afferent fibers) and a potent downregulator of the immune response (via efferent fibers). The efferent pathway mediates the Cholinergic Anti-Inflammatory Pathway (CAP), an essential neurophysiological reflex. Upon activation, the Vagus Nerve releases Acetylcholine (ACh), which binds to the alpha 7 nicotinic Acetylcholine Receptor (α7nAChR) on immune cells (macrophages). This interaction initiates an inhibitory cascade, suppressing the nuclear translocation of NF-kappa-beta and thereby inhibiting the release of key pro-inflammatory cytokines such as Tumor Necrosis Factor alpha (TNF-alpha) and Interleukin-6 (IL-6). Dysfunction in vagal tone is strongly correlated with increased disease activity and inflammation in IBD, chronic pain, and neurodegenerative disorders. Given its vital role, the Vagus Nerve has emerged as a promising therapeutic target. Strategies like Invasive and Non-Invasive Vagus Nerve Stimulation (VNS), particularly Transcutaneous Auricular VNS (tVNS), are actively being investigated for their potential to restore parasympathetic balance and leverage the CAP to mitigate systemic inflammation. Furthermore, behavioral techniques and microbiota-modulating interventions that boost SCFA production act as indirect vagal enhancers. The Vagus Nerve thus represents a critical frontier in bioelectronic medicine for developing non-pharmacological, targeted treatments for inflammation-driven pathologies. |
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