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March 2008 Off the Wire . . .




The CB2 cannabinoid receptor controls myeloid progenitor trafficking. Involvement in the pathogenesis of an animal model of multiple sclerosis.

Article Date: 2008 Mar 11

Biochemistry and Molecular Biology I, Complutense University, School of Biology, Madrid 28040.

Cannabinoids are potential agents for the development of therapeutic strategies against multiple sclerosis. Here we analyzed the role of the peripheral CB2 cannabinoid receptor in the control of myeloid progenitor cell trafficking towards the inflamed spinal cord and their contribution to microglial activation in an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis, EAE). CB2 receptor knock-out mice showed an exacerbated clinical score of the disease when compared to their wild-type littermates, and this occurred in concert with extended axonal loss, T-lymphocyte (CD4+) infiltration and microglial (CD11b+) activation. Immature bone marrow-derived CD34+ myeloid progenitor cells, which play a role in neuroinflammatory pathologies, were shown to express CB2 receptors and to be abundantly recruited towards the spinal cords of CB2 knock-out EAE mice. Bone marrow-derived cell transfer experiments further evidenced the increased contribution of these cells to microglial replenishment in the spinal cords of CB2-deficient animals. In line with these observations, selective pharmacological CB2 activation markedly reduced EAE symptoms, axonal loss and microglial activation. CB2 receptor manipulation altered the expression pattern of different chemokines (CCL2, 3, 5) and their receptors CCR1, 2), thus providing a mechanistic explanation for its role in myeloid progenitor recruitment during neuroinflamation. These findings demonstrate the protective role of CB2 receptors in EAE pathology; provide evidence for a new site of CB2 receptor action, namely the targeting of myeloid progenitor trafficking and its contribution to microglial activation; and support the potential use of non-psychoactive CB2 agonists in therapeutic strategies for multiple sclerosis and other neuroinflammatory disorders.

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