Macrophage recruitment signals following unilateral chorda tympani nerve degeneration/

Abstract

The chorda tympani nerve ( CT) innervates taste buds within fungiform papillae. Unilateral transaction 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)-1a 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 dpes · not alter taste · ;;function. Other adhesion molecules may be able to compensate for the loss of 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.