Abstract
Acute ischemic and traumatic injury of the central nervous system (CNS) is known to induce a cascade of inflammatory events that lead to secondary tissue damage. In particular, the sterile inflammatory response in stroke has been intensively investigated in the last decade, and numerous experimental studies demonstrated the neuroprotective potential of a targeted modulation of the immune system. Among the investigated immunomodulatory agents, intravenous immunoglobulin (IVIg) stand out due to their beneficial therapeutic potential in experimental stroke as well as several other experimental models of acute brain injuries, which are characterized by a rapidly evolving sterile inflammatory response, e.g., trauma, subarachnoid hemorrhage. IVIg are therapeutic preparations of polyclonal immunoglobulin G, extracted from the plasma of thousands of donors. In clinical practice, IVIg are the treatment of choice for diverse autoimmune diseases and various mechanisms of action have been proposed. Only recently, several experimental studies implicated a therapeutic potential of IVIg even in models of acute CNS injury, and suggested that the immune system as well as neuronal cells can directly be targeted by IVIg. This review gives further insight into the role of secondary inflammation in acute brain injury with an emphasis on stroke and investigates the therapeutic potential of IVIg.
Highlights
Reviewed by: Arthur Liesz, Ludwig-Maximilians-Universität München, Germany Anna Fogdell-Hahn, Karolinska Institutet, Sweden Andreas Meisel, Charité Universitätsmedizin Berlin, Germany
Several experimental studies implicated a therapeutic potential of intravenous immunoglobulin (IVIg) even in models of acute central nervous system (CNS) injury, and suggested that the immune system as well as neuronal cells can directly be targeted by IVIg
IVIg treatment of primary neuronal cultures subjected to simulated ischemia for 12 h significantly reduced protein levels of factors involved in neuronal cell death like the phospho-SAPK c-Jun NH2terminal kinase (p-JNK) and phospho-p65 NFκB and inhibited the loss of the neuronal marker microtubulin associated protein 2 (MAP2) [147, 158]
Summary
Reviewed by: Arthur Liesz, Ludwig-Maximilians-Universität München, Germany Anna Fogdell-Hahn, Karolinska Institutet, Sweden Andreas Meisel, Charité Universitätsmedizin Berlin, Germany. Acute ischemic and traumatic injury of the central nervous system (CNS) is known to induce a cascade of inflammatory events that lead to secondary tissue damage. Among the investigated immunomodulatory agents, intravenous immunoglobulin (IVIg) stand out due to their beneficial therapeutic potential in experimental stroke as well as several other experimental models of acute brain injuries, which are characterized by a rapidly evolving sterile inflammatory response, e.g., trauma, subarachnoid hemorrhage. Several experimental studies implicated a therapeutic potential of IVIg even in models of acute CNS injury, and suggested that the immune system as well as neuronal cells can directly be targeted by IVIg. This review gives further insight into the role of secondary inflammation in acute brain injury with an emphasis on stroke and investigates the therapeutic potential of IVIg. Acute tissue damage is known to trigger a highly conserved cascade of inflammatory events. In addition to inflammation associated with acute injuries, there is convincing evidence for the importance of chronic inflammatory processes in degenerative diseases of the brain, including Parkinson’s and Alzheimers disease [4]
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