Cytokines and Pain
Within the past few years, it has become recognized that the immune system communicates to the brain. Substances released from activated immune cells (cytokines) stimulate peripheral nerves, thereby signaling the brain and spinal cord that infection/inflammation has occurred. Additionally, peripheral infection/inflammation leads to de novo synthesis and release of cytokines within the brain and spinal cord. Thus, cytokines effect neural activation both peripherally and centrally. Through this communication pathway, cytokines such as interleukin-1, interleukin-6 and tumor necrosis factor markedly alter brain function, physiology and behavior. One important but underrecognized aspect of this communication is the dramatic impact that immune activation has on pain modulation. The purpose of this book is to examine, for the first time, immune-to-brain communication from the viewpoint of its effect on pain processing. It is aimed both at the basic scientist and health care providers, in order to clarify the major role that substances released by immune cells play in pain modulation. This book contains chapters contributed by all of the major laboratories focused on understanding how cytokines modulate pain. These chapters provide a unique vantage point from which to examine this question, as the summarized work ranges from evolutionary approaches across diverse species, to the basics of the immune response, to the effect of cytokines on peripheral and central nervous system sites, to therapeutic potential in humans.
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Overview of inflammatory cytokines and their role in pain
Evolutionary perspectives of cytokines in pain
Mediators mechanisms and implications
Hyperalgesia from subcutaneous cytokines
Cytokinenerve growth factor interactions in inflammatory hyperalgesia
Hyperalgesic actions of cytokines on peripheral nerves
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acid action activity afferent allodynia analgesia anti-hyperalgesic anti-inflammatory antibodies Aplysia arthritis astrocytes axons behaviors binding bradykinin Brain Res carrageenin central CFA-induced concentrations cytokines dexamethasone Dinarello dorsal root dose effects expression Ferreira SH fibroblasts gene glia glial hemocytes human hyper hyperalgesia hyperalgesic responses hypersensitivity i.c.v. injection i.pl IL-1 receptor illness responses Immunol increase indomethacin induced hyperalgesia inflammation inflammatory hyperalgesia inhibited inhibitors interleukin-1 involved ipsilateral kinase lesion Lys-D-Pro-Thr macrophages Maier SF mast cells mechanical hyperalgesia mediators mice microglia models mRNA nerve growth factor nerve injury neuropathic pain neuropeptide Neurosci nitric oxide nociceptive nociceptors pathways peptide peripheral nerve pg/kg PGE2 Pharmacol Proc Natl Acad production proinflammatory cytokines prostaglandin protein receptor antagonist release rhIL-1p role Schwann cells sciatic nerve sensitivity sensory neurons serum signal spinal cord stimulation synovial synthesis thermal hyperalgesia tion tissue TNFa tumor necrosis factor upregulation Wallerian degeneration Watkins LR