The differential role of spinal MHC class II and cellular adhesion molecules in peripheral inflammatory versus neuropathic pain in rodents.

The present study was designed to determine the role of central expression of immunoregulatory molecules in the development and maintenance of allodynia following a peripheral inflammatory insult or nerve transection. Differential spinal expression of major histocompatibility complex (MHC) class II, platelet-endothelial cellular adhesion molecule (PECAM), intercellular adhesion molecule (ICAM) and CD4 was observed in the two injury models. Intraplantar zymosan produced transient allodynia and only PECAM and ICAM immunoreactivity. In contrast, persistent mechanical allodynia and enhanced spinal PECAM, ICAM, MHC class II and CD4 immunoreactivity was observed following peripheral nerve transection. MHC class II knockout mice exhibited attenuated allodynia following spinal nerve transection as compared to wild-type control mice. These findings suggest that central neuroimmune activation may contribute to the maintenance of neuropathic pain following peripheral L5 spinal nerve transection but not following a peripheral inflammatory insult.