Figure 1.

Depiction of the evolvement and amplification of postischemic inflammation. Hypoxia and glucose deprivation cause severe cell damage and dying cells release DAMPS and ROS, which activate resident immune cells. Subsequent production of inflammatory cytokines contributes to the breakdown of the blood–brain-barrier (BBB) and promotes the infiltration of cells of the adaptive as well as innate immunity, which cause a severe inflammatory response and deteriorate the initial brain damage.