Research Summary
Using molecular, cellular, and in vivo pharmacological approaches, my work is focused on spinal mechanisms through which inflammatory processes
lead to chronic pain states. Of particular interest is the role of spinal glia cells in pain processing. For example, my work has shown that
the p38-&beta mitogen activated protein kinase isoforms is uniquely expressed in microglia and that this kinase is phosphorylated in spinal microglia
in response to peripheral injury and inflammation.
The participation of lipid mediators in the communication between microglia and neurons in conditions of persistent pain is currently being
investigated. In addition, the contribution of spinal anti-inflammatory signaling pathways are being studied. One family of such lipid mediators
are the lipoxins, know to have important anti-inflammatory properties in the periphery. The overall aim with my work is to further understand how
non-neuronal cells mediate spinal sensitization and to examine the role of spinal anti-inflammatory processes pathways in the regulated of persistent
pain states.
Publications
Svensson CI, Marsala M, Westerlund A, Calcutt NA, Campana WM, Freshwater JD, Catalano R, Feng Y, Protter AA, Scott B, Yaksh TL. Activation of p38 mitogen-activated protein kinase in spinal microglia is a critical link in inflammation-induced spinal pain processing. Journal of Neurochemistry. 2003 Sep;86(6):1534-44
Svensson CI, Killerman Lucas K, Hua XY, Dennis EA, Yaksh TL. Spinal PhospholipaseA2 in Inflammatory Hyperalgesia: Role of the small, secreted sPLA's. Neuroscience. 2005; 133(2):543-53
Svensson CI, Fitzsimmons B, Azizi S, Powell HC, Hua XY, Yaksh TL. Spinal p38b isoform mediates tissue injury-induced hyperalgesia and spinal sensitization. J Neurochemistry. 2005 Mar;92(6):1508-20
Svensson CI, Zattoni M, Serhan CN. Lipoxins and aspirin-triggered lipoxin inhibit inflammatory pain processing. J Exp Med. 2007 Jan 22;[E-pub ahead of print]
