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Intriguingly, urokinase-type plasminogen activator uPA , which is commonly used in the treat- ment of ischemic stroke, has been demonstrated to increase the expression of several cytokines, among which is CX3CL1 Lee et al. Considering the protective effect of CX3CL1, this led to the hypothesis that the activity of this thrombolytic substance goes far behind its very well known role as plasminogen activator in stroke therapy. In brain ischemia, glutamate-induced excitotocixity is involved in the modula- tion of neuronal cell death. Under hypoxic conditions, astrocytes down-regulate CX3CL1 expression while up-regulate other cytokines and chemokines potentially involved in the migration of neuronal precursors towards hypoxic regions to replace the damaged cells Xu et al.
The cerebrospinal fluid CSF of patients affected with different central and peripheral neuroinflammatory diseases contains an increased amount of CX3CL1 compared with patients with non-inflam- matory neurological diseases Kastenbauer et al.
Results obtained in these experiments led to the suggestion that neuron injury, causing CX3CL1 release, could recruit microglial cells in the damaged area taking part to the reparative or destructive processes. When, 2 years later Jung et al. In line with this evidence, CX3CL1 in the brain has in general an inhibitory activity on microglia function, in terms of inflammatory cytokine release while, in the spinal cord, CX3CL1 stimulates the release of cytokines from microglia. Overall, considering the data described in this chapter, at this stage of knowledge CX3CL1 could be considered as a neuronal messenger, whose soluble form increases upon several kinds of toxic stimuli, primarily acting on microglial cells in a way that could differ as a consequence of the local cytokine milieu, possibly regu- lating the activation and the potential toxicity of microglia.
Acknowledgments The authors thank Drs. Fabrizio Eusebi and Flavia Trettel for helpful discus- sions during the writing of this chapter. J Immunol — Cambien B, Pomeranz M, Schmid-Antonmarchi H et al Signal transduction pathways involved in soluble fractalkine-induced monocytic cell adhesion. Nat Neurosci — Chapman GA, Moores K, Harrison D et al Fractalkine cleavage from neuronal membranes represents an acute event in the inflammatory response to excitotoxic brain damage.
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Mol Neurobiol — Deiva K, Geeraerts T, Salim H et al Fractalkine reduces N-methyl-d-aspartate-induced calcium flux and apoptosis in human neurons through extracellular signal-regulated kinase activation. Cell — Ji JF, He BP, Dheen ST et al Interaction of chemokines and chemokine receptors mediate the migration of mesenchymal stem cells to the impaired site in the brain after hypoglossal nerve injury. J Neuroimmunol —12 Johnston IN, Milligan ED, Wieseler-Frank J et al A role for proinflammatory cytokines and fractalkine in analgesia, tolerance, and subsequent pain facilitation induced by chronic intrath- ecal morphine.