Astrid E. Cardona Ph.D.
Assistant Professor of Neuroimmunology & Fractalkine Receptor Biology
Office: MBT 1.216
Email: astrid.cardona@utsa.edu
Ph.D., University of Texas Health Science Center at San Antonio, 2002
B.Sc., University of Antioquia, Colombia, 1996
Research Interests
Our studies use experimental autoimmune encephalomyelitis (EAE) as a model to investigate pathological events related to Multiple Sclerosis. The primary focus is to determine the contribution of the fractalkine receptor (CX3CR1) to disease severity.
Fractalkine (CX3CL1) and its receptor CX3CR1 provide a physiologically-relevant neuron-microglia communication mechanism. Fractalkine is a unique central nervous system (CNS) chemokine present on neuronal membranes and capable of being released as a soluble protein by constitutive or stress-activated ADAM-family protease activity. Fractalkine exerts its functions by binding to CX3CR1 on microglial cells. Although they are mainly produced in the CNS, Fractalkine and CX3CR1 also have a distinctive peripheral pattern of expression. Fractalkine is found at low levels in endothelial and some epithelial cells of selected tissues such as kidney, lung, prostate and heart, but not spleen or liver. CNS endothelial cells do not express fractalkine. Circulating monocytes, dendritic cells and NK cells express CX3CR1. In vitro studies suggested that soluble fractalkine mediates microglial chemoattraction but, surprisingly inhibits microglial activation, and protects microglia from apoptosis. Some of the questions we are addressing include: Does CX3CR1 play a role in the trafficking of microglial precursors? Does CX3CR1-deficiency on microglia or peripheral cells enhance neuronal/axonal pathology? How does CX3CR1-deficiency alter CNS immune responses? We intend to clarify the role of fractalkine/CX3CR1 in the brain, research that is instrumental for potential development of therapeutic agents
Recent Publications
Huang, D., J. Wujek, G. Kidd, A.E. Cardona, T. He, M.E. Sasse, E. Stein, J. Kish, I. F. Charo, A. Proudfoot, B. J. Rollins, T. Handel, and R.M. Ransohoff . Chronic expression of monocyte chemoattractant protein-1 in the central nervous system causes delayed encephalopathy and altered microglial function in mice. 2005. FASEB J. 19(7):761-772.
Cardona, AE., Pioro E., Sasse M, Kostenko V., Cardona S., Dijkstra I. , Huang D, Kidd G, Dombrowski S, Dutta R, Lee JC, Cook DN, Jung S, Lira SA, Littman DR, Ransohoff RM. Control of microglial neurotoxicity by the fractalkine receptor. 2006. Nat Neurosci. 9(7):917-924.
Rebenko-Moll, N., Liu, L, Cardona A., Ransohoff, RM. How mononuclear cells enter and exit the nervous system: Role of chemokines. 2006. Curr.Opin.Immunol. 18:683-689.
Cardona, AE., Huang, D., Sasse, M. and Ransohoff, RM. Isolation of murine microglial cells for RNA analysis or flow cytometry. 2006. Nat. Protoc. 1(4):1947-1951.
Cardona, AE. and Ransohoff RM. Chemokine receptors in neuroinflammation. In: The chemokine receptors. JK Harrison and NW Lukas, editors. Humana Press, Totowa, NJ. 2007.
Ransohoff RM, Liu L and Cardona AE. 2007. Chemokines and chemokine receptors: multipurpose players in neuroinflammation. Int. Rev. Neurobiol. 82:187-204.
Cardona AE, Sasse ME, Mizutani M, Cardona SM, Liu L, Savarin C, Hu T and Ransohoff RM. 2008. Scangenging roles of chemokine receptors: chemokine receptor deficiency is associated with increased levels of ligand in circulation and tissues. Blood. July 15; 112(2):256-263.
Cardona AE, Li M, Liu L, Savarin C and Ransohoff RM. 2008. Chemokines in and out of the central nervous system: much more than chemotaxis and inflammation. J. Leukoc. Biol. 84(3):587-94.