Accumulating evidence during the last decade has shown that the CNS can mount a well-defined inflammatory reaction to a variety of insults including @entity130 , @entity63 , transplantation, @entity1800 as well as @entity179 . Many aspects of this centrally derived inflammatory response parallel to some extent the nature of such a reaction in the periphery. Through the recent application of molecular genetic techniques including PCR, utilization of cDNA probes in conjuncture with the availability of highly specific antibodies, new concepts are rapidly emerging as to the molecular mechanisms associated with the development of @entity1545 . In particular, the importance of cytokines, especially @entity310 and @entity1356 , is emphasized in the propagation and maintenance of a CNS inflammatory response. This review summarizes evidence in support of a case for @entity63 and @entity130 eliciting an inflammatory condition in the injured brain. The inflammatory condition consists of cells ( @entity5309 early after the onset of @entity1545 and subsequently monocyte infiltration) and mediators (cytokines, chemokines and adhesion molecules). It is clear that de novo up-regulation of pro-inflammatory cytokines, chemokines and endothelial-leukocyte adhesion molecules in the brain occurs soon following focal @entity63 and @entity130 and at a time when the tissue injury is evolving. The significance of the inflammatory response and its contribution to @entity1545 are now becoming better understood. Evidence has emerged in support of the role of cytokines in driving the inflammatory response and that this process is causally related to the degree of @entity1545 . Evidence reviewed includes: (1) the capacity of specific cytokines to exacerbate @entity75 ; (2) the capacity of specific cytokine blockade to reduce @entity63 @entity75 ; (3) depletion of circulating @entity5309 reduces @entity2806 , and (4) antagonists of the endothelial-leukocyte adhesion interactions (e.g. anti- @entity2071 ) reduce @entity2806 . Targeting the cytokines that drive the brain inflammatory response to injury provides opportunities to intervene with novel therapeutics in @entity64 and neurotrauma.

The role of cytokines in the neuropathology of XXXX and neurotrauma.

@entity1545 :: ('MESH:D020214', 'Disease') :: ['brain injury'] @entity64 :: ('MESH:D020521', 'Disease') :: ['stroke'] @entity2806 :: ('MESH:D002545', 'Disease') :: ['ischemic brain injury'] @entity63 :: ('MESH:D007511', 'Disease') :: ['ischemia', 'ischemic'] @entity310 :: ('7124', 'Gene') :: ['TNFalpha'] @entity1356 :: ('3553', 'Gene') :: ['IL-1beta'] @entity75 :: ('MESH:D001927', 'Disease') :: ['brain damage'] @entity1800 :: ('MESH:D014777', 'Disease') :: ['viral infections'] @entity179 :: ('MESH:D019636', 'Disease') :: ['neurodegeneration'] @entity5309 :: ('MESH:C564275', 'Disease') :: ['neutrophils'] @entity2071 :: ('3383', 'Gene') :: ['ICAM-1'] @entity130 :: ('MESH:D014947', 'Disease') :: ['trauma']
@entity64 :: (MESH:D020521,Disease) :: ['stroke']
