N , reveals a lack of Mac-1 cells to sites of Acanthamoeba focus in the brains of infected M were Mice treated with eZ-9-THC compared with vehicle-treated contr Acanthamoeba infection. These findings demonstrate that microglia, either do not migrate to the infected areas or have been selectively Camptothecin targeted and destroyed Destroyed by Acanthamoeba. Entered the treatment of newborn rats cortical cultures with microglia-EZ-9 THC Born inhibition of migratory response to Acanthamoeba conditioned medium, the proteases and other factors, ben Am, Which serve as chemotactic stimuli released contains Lt In addition, treatment with the potent agonist CP55940 CB1/CB2 has entered Born a significant decrease in the concentration on the migration of microglia in response to CM.
The highly CB2 selective ligands O in 2137 had a profound and significant inhibition was in response to CM microglial migration may need during the treatment with ACEA CB1-selective ligands have a minimal effect. Closing Lich did treatment of microglia with the CB1 antagonist SR141716A Cabral and Thomas Griffin Expert XL880 Rev Mol Med 12 page manuscript author, increases available in PMC 2010, the first January. PA Author Manuscript NIH-PA Author Manuscript block NIH Manuscript NIH-PA Author is not the inhibitory effect of CP55940 w Led during the treatment with the CB2 antagonist SR144528 to reverse the inhibitory effect of CP55940. These collective results showed that the inhibition mediated by cannabinoid CM of microglia stimulated response to A.
culbertsoni in the brain of M Was brought nozzles in combination, at least partially, to the CB2. By whiche mode -9 THC and other cannabinoid Be inhibited by exogenous factors such as CP55940 signal by the CB2 chemotactic response of microglia Acanthamoeba yet defined. However, it is known to generate that affect proteases, phospholipases Acanthamoeba and other factors, the phospholipids in microglia k Can membranes, the fission products. It is postulated that the bioactive lipid mediators generated go Ren endocannabino 2-AG run, chemotaxis by activating autocrine / paracrine CB2 is used. The cannabinoid Exogenous EZ-9-THC, k Can these costimulatory molecules and chemotactic response of other chemotactic stimuli, transductional by superimposing an inhibitory effect on the subsequent activation of the signal CB2.
The hei t, k EZ-9 THC Nnte the synthesis and / or inhibit Ver Publication by two AG or, alternatively, by its relatively long half-life compared to the AG 2, they anticipate endocannabino The ligation of CB2. RESEARCH QUESTIONS In summary, research in progress and OUTSTANDING There are currently many data indicating that CB2 plays a role The functional relevance in inflammation. The r Is particularly evident for the cells of the myeloid lineage Of confinement Lich macrophages and macrophages, and resident microglia in the CNS. The latter cells are morphologically, ph Notypisch related and functionally to macrophages. The CB2 is different from macrophages and macrophage Like cells, wherein the h Chsten values detected when these cells expressed hypersensitive and in the reports surface Surface, indicating the presence of a functional relevance of the time window in which the activation of macrophages CB2 module activity Ten. Signature of activity Th and respond primedmacrophages chemotaxis and antigen processing, respectively. The system endocannabino 2 AG, macrophages and microglia caused Duri