Abstract
Recent studies have demonstrated a pronounced influence by the autonomic nervous system on immune-mediated experimental hepatitis in the mouse. Adrenergic sympathetic neurons alleviate while capsaicin-sensitive peptidergic primary afferent neurons aggravate liver injury. This was evidenced by recording morphological and functional parameters upon chemical sympathectomy and application of beta-adrenergic agonists, and capsaicin depletion of afferents, neurokinin receptor antagonists, and application of exogenous substance P, respectively. These phenomena are most likely based on close anatomical relationships between nerve fibers and various immune cells in the liver. Modulation of autonomic nervous system functions may open novel therapeutic strategies in immune and inflammatory liver diseases.
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