The chorda tympani nerve (CT) innervates taste buds within fungiform papillae. Unilateral transection of the CT causes degeneration of the ipsilateral taste buds and a bilateral increase in activated lingual macrophages. However, dietary Na+ restriction prevents the macrophage response and results in a subnormal neural response to Na+ stimuli by the contralateral, intact CT. Stimulating immune system function with lipopolysaccharide (LPS) restores the bilateral macrophage response to CT section in Na +-restricted rats. This macrophage response is associated with the recovery of normal taste function, suggesting that macrophages affect taste function. Intracellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and monocyte chemoattractant protein (MCP)-1 are upregulated prior to and during the peak macrophage response suggesting that these molecules are recruitment signals for macrophage entry following CT injury. Macrophage inflammatory protein (MIP)-1alpha is not significantly upregulated following CT section. Importantly, the increase in VCAM-1 expression is prevented by dietary Na+ restriction, which may partially explain the decreased macrophage response in these animals. However, binding of an antibody against platelet endothelial cell adhesion molecule (PECAM)-1, which is downstream of ICAM-1 and VCAM-1, paradoxically increases macrophage recruitment and does not alter taste function. Other adhesion molecules may be able to compensate for the loss of PECAM-1. The response of the immune system to CT section is diverse and requires the cooperation of many molecules in order to recruit macrophages to maintain normal taste function. ICAM-1, VCAM-1, and MCP-1 are upstream recruitment signals for macrophages that may ultimately affect the function of taste receptor cells.; Index words. ICAM-1, VCAM-1, MCP-1, MIP-1alpha, Macrophage, Chorda Tympani Nerve, Lipopolysaccharide, Dietary Sodium Restriction, Neuroimmune Interactions.
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