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- W2015160992 abstract "The endocannabinoid system is suggested to control neuroinflammatory responses and therefore harbors potential for the treatment of parasite-induced CNS infections, such as cerebral malaria (CM). We investigated the role of the cannabinoid receptor 2 (CB2) in the pathogenesis of a CM mouse model. CB2 knockout (Cnr2−/−) mice inoculated with Plasmodium berghei ANKA-erythrocytes (PbA-RBC) exhibited enhanced survival, while wild-type controls succumbed to disease. Cnr2−/− mice showed a reduced parasite load in the brain and a diminished blood–brain-barrier disruption. Therapeutic application of a specific CB2 antagonist conferred increased CM resistance in C57BL/6 mice, while CB2-expressing myeloid-derived cells contributed to enhanced susceptibility to CM in mixed bone marrow-chimeras. Myeloid cells expressing enhanced levels of IL-10, arginase-1 and mannose receptors (MMR) accumulated in the Cnr2−/− spleens. Accordingly, brain infiltrates of Cnr2−/− mice contained increased percentages of Ly6Chigh CD11b+ myeloid cells that expressed enhanced MMR and arginase-1, distinctive markers of anti-inflammatory macrophage functions. The M2-macrophage chemokine CCL17 was identified as the essential factor that mediated enhanced protection against CM in the absence of CB2, since CCL17xCnr2 double-deficient mice were fully susceptible to CM. Thus, targeting CB2 may be a promising approach for the development of alternative treatment regimes of CM." @default.
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- W2015160992 date "2014-10-01" @default.
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- W2015160992 title "CB2 modulates susceptibility to experimental cerebral malaria through a CCL17-dependent mechanism" @default.
- W2015160992 doi "https://doi.org/10.1016/j.jneuroim.2014.08.197" @default.
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