Neuronal MCP-1 expression in response to remote nerve injury

Direct injury of the brain is followed by inflammatory responses regulated by cytokines and chemoattractants secreted from resident glia and invading cells of the peripheral immune system. In contrast, after remote lesion of the central nervous system, exemplified here by peripheral transection or c rush of the facial and hypoglossal nerve, the locally observed inflammatory activation is most likely triggered by the damaged cells themselves, that is, the injured neurons. The authors investigated the expression of the che moattractants monocyte chemoattractant protein MCP-1. regulation on activat ion normal T-cell expressed and secreted (RANTES), and interferon-gamma ind ucible protein IP10 after peripheral nerve lesion of the facial and hypoglo ssal nuclei. In situ hybridization and immunohistochemistry revealed an ind uction of neuronal MCP-1 expression within 6 hours postoperation, reaching a peak at 3 days and remaining up-regulated for up to 6 weeks. MCP-1 expres sion was almost exclusively confined to neurons but was also present on a f ew scattered glial cells. The authors found no alterations in the level of expression and cellular distribution of RANTES or IP10, which were both con fined to neurons. Protein expression of the MCP-1 receptor CCR2 did not cha nge. MCP-1, expressed by astrocytes and activated microglia, has been shown to be crucial for monocytic, or T-cell chemoattraction, or both. According ly, expression of MCP-1 by neurons and its corresponding receptor in microg lia suggests that this chemokine is involved in neuron and microglia intera ction.