Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. Export

@article{citeulike:6087056, abstract = {Macrophages dominate sites of CNS injury in which they promote both injury and repair. These divergent effects may be caused by distinct macrophage subsets, i.e., "classically activated" proinflammatory (M1) or "alternatively activated" anti-inflammatory (M2) cells. Here, we show that an M1 macrophage response is rapidly induced and then maintained at sites of traumatic spinal cord injury and that this response overwhelms a comparatively smaller and transient M2 macrophage response. The high M1/M2 macrophage ratio has significant implications for CNS repair. Indeed, we present novel data showing that only M1 macrophages are neurotoxic and M2 macrophages promote a regenerative growth response in adult sensory axons, even in the context of inhibitory substrates that dominate sites of CNS injury (e.g., proteoglycans and myelin). Together, these data suggest that polarizing the differentiation of resident microglia and infiltrating blood monocytes toward an M2 or "alternatively" activated macrophage phenotype could promote CNS repair while limiting secondary inflammatory-mediated injury.}, author = {Kigerl, Kristina A. and Gensel, John C. and Ankeny, Daniel P. and Alexander, Jessica K. and Donnelly, Dustin J. and Popovich, Phillip G.}, citeulike-article-id = {6087056}, citeulike-linkout-0 = {http://dx.doi.org/10.1523/JNEUROSCI.3257-09.2009}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19864556}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19864556}, comment = {macrophage subset is associated with spinal cord regeneration}, day = {28}, doi = {10.1523/JNEUROSCI.3257-09.2009}, issn = {1529-2401}, journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience}, keywords = {m2, macrophage, regeneration, spinal}, month = {October}, number = {43}, pages = {13435--13444}, posted-at = {2009-11-09 04:58:03}, priority = {2}, title = {Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord.}, url = {http://dx.doi.org/10.1523/JNEUROSCI.3257-09.2009}, volume = {29}, year = {2009} }

TY - JOUR ID - citeulike:6087056 L3 - citeulike-article-id:6087056 N2 - Macrophages dominate sites of CNS injury in which they promote both injury and repair. These divergent effects may be caused by distinct macrophage subsets, i.e., "classically activated" proinflammatory (M1) or "alternatively activated" anti-inflammatory (M2) cells. Here, we show that an M1 macrophage response is rapidly induced and then maintained at sites of traumatic spinal cord injury and that this response overwhelms a comparatively smaller and transient M2 macrophage response. The high M1/M2 macrophage ratio has significant implications for CNS repair. Indeed, we present novel data showing that only M1 macrophages are neurotoxic and M2 macrophages promote a regenerative growth response in adult sensory axons, even in the context of inhibitory substrates that dominate sites of CNS injury (e.g., proteoglycans and myelin). Together, these data suggest that polarizing the differentiation of resident microglia and infiltrating blood monocytes toward an M2 or "alternatively" activated macrophage phenotype could promote CNS repair while limiting secondary inflammatory-mediated injury. IS - 43 JF - The Journal of neuroscience : the official journal of the Society for Neuroscience SN - 1529-2401 EP - 13444 TI - Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. VL - 29 SP - 13435 KW - m2 KW - macrophage KW - regeneration KW - spinal N1 - macrophage subset is associated with spinal cord regeneration AU - Kigerl, Kristina AU - Gensel, John AU - Ankeny, Daniel AU - Alexander, Jessica AU - Donnelly, Dustin AU - Popovich, Phillip PY - 2009/10/28/ UR - http://dx.doi.org/10.1523/JNEUROSCI.3257-09.2009 ER -