Induction of interleukin-1β mRNA after focal cerebral ischaemia in the rat

Reduced Ischemic Brain Injury in Interleukin-1β Converting Enzyme—Deficient Mice

“…There is considerable evidence that ICE and IL-I !3/IL-I ra mRNA levels are acutely increased in cerebral ischemia (Buttini et a!., 1994;Liu et a!., 1993;Wang et a!., 1994), in the microglia and astrocytes and endothelial cells but not neurons (Bhat et aI., 1996;Lynch et aI., 1997). The first demonstration that IL-113 mediates ischemic brain dam age was the finding that intracerebroventricular injection of the antagonist protein, IL-I ra, reduced stroke size in rats by 50% (Loddick and Rothwell, 1996;ReIton and Rothwell, 1992).…”

Soluble TNF Receptor 1-Secreting ex Vivo-Derived Dendritic Cells Reduce Injury After Stroke

“…After ischemia, messenger RNA expression of potent inflammatory cytokines and chemokines TNF-a, IL-1b, and MCP-1 increases in the brain within 1 to 3 hours and peaks between 24 and 36 hours. [4][5][6][7][8][9][10] Increases in protein levels of these factors occur by 6 hours after stroke (ref. 4 and our data) in neurons, glia, peripheral immune organs, and circulating immune cells.…”

Inhibition of interleukin 1β converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage

“…A role for apoptosis in ischemic injury was proposed based on morphological (terminal deoxynucleotidyltransferase-mediated UTP end labeling staining) and biochemical (DNA fragmentation) evidence (4,5,11). Moreover, IL-1␤ mRNA and protein expression increases in ischemic tissue during permanent focal (12,13) and global ischemia (14,15). Endogenously produced mature IL-1␤ plays an important role in hypoxia-mediated apoptosis in vitro (16).…”