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- W2897822557 abstract "OBJECTIVE: To investigate the effects of A2a receptor (A2aR) on the blood brain barrier (BBB) integrity in MS BACKGROUND: MS is an autoimmune disease of the CNS characterized in part by a CD4+ Th1 lymphocyte-mediated autoimmune response, inflammatory cell infiltration and demyelination in the CNS, and progressive and recurrent impairment. Th1 cytokines are key factors in the regulation of inflammatory responses correlated with the loss of blood brain barrier (BBB) integrity.Adenosine acting at its receptors, is a potent endogenous regulator of inflammation. Adenosine prevents the increase in vascular permeability and promotes endothelial barrier function. We investigated the effects of A2aR manipulation on Th1 cytokines. DESIGN/METHODS: MS brain tissue obtained from UCLA were used to detect A2aR expression in MS lesions. We examined the distribution of F-actin and the expression of tight junction proteins in cultured endothelial cells treated with Th1 cytokines or Th1 cytokines plus specific A2aR agonist (CGS21680). C57BL/6 mice were immunized by myelin oligodendrocyte glycoprotein (MOG35-55) to induce experimental autoimmune encephalomyelitis (EAE) and then given CGS21680 by i.p. daily. Neurological impairment was evaluated using disease scores. BBB permeability was measured by the content of fluorescent tracers, sodium fluoride (Na-F)in CNS after i.p. injection and FITC-dextran in CNS after i.v. injection. RESULTS: A2aR is expressed by endothelial cells in human MS and mice EAE lesions. Th1 cytokines caused the disturbance of cytoskeleton and a decrease of tight junction proteins. A2aR specific agonist prevents endothelial cells from injury caused by Th1 cytokines in vitro. A2aR specific agonist CGS21680(100ng/kg,i.p.) ameliorates neuro-inflammation and neuro-behavioral deficits in vivo, and decreases the BBB permeability in EAE. CONCLUSIONS: Activation of the A2aR exerts a strong protection on BBB from increased permeability caused by Th1 cytokines. Our results indicated that A2aR agonists could represent a novel therapeutic tool for MS treatment. Study Supported by: Shubert Foundation Disclosure: Dr. Alahiri has nothing to disclose. Dr. Liu has nothing to disclose. Dr. Ulloa has nothing to disclose. Dr. Sadiq has nothing to disclose." @default.
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- W2897822557 date "2015-04-06" @default.
- W2897822557 modified "2023-09-22" @default.
- W2897822557 title "The Protection of A2aR on BBB Permeability from Th1 Cytokines in MS (P2.202)" @default.
- W2897822557 hasPublicationYear "2015" @default.
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