Chapter 3.6 - Cell Recruitment in the Axotomized Facial Nucleus: Role of Cytokines, Chemokines and Cell Adhesion Molecules

Abstract

This chapter describes the different forms of cellular recruitment in injury model, summarizes the current data on the associated molecular mechanisms, and briefly discusses the biological function subserved by highly conserved cellular response. After injury, the ramified microglia transforms rapidly from a resting to an activated state, with an increase in cell body size, a thickening of proximal processes, and decreased ramification of the distal branches. On the molecular level, this activation proceeds through a series of step: the first is the early state of alert; followed by homing and adhesion, phagocytosis; and, finally, the bystander activation of the neighboring non-phagocytic cells. These activated microglias are strongly attracted by damaged neurons, but in two different ways. Recent molecular studies also show that these microglial responses are controlled by quite different signaling pathways. Early stages of microglial activation and lymphocyte recruitment are dependent on macrophage colony stimulating factor (MCSF) and interleukin-6 (IL6), and the late phase on IL1, tumor necrosis factor (TNF) and their receptors. A number of chemokines such as fractalkine (CX3CL1) and macrophage chemoattractant protein-1 or MCP1 (CCL2) are also strongly upregulated in the aftermath of nerve injury and may play a pivotal role in recruiting different cell types.