Induction of cytokines, chemokines and adhesion molecule mRNA in a rat forebrain reperfusion model.

Cellular damage secondary to reperfusion following ischemic insult has been hypothetically attributed to an inflammatory cascade concerted by cell-to-cell interactions. While the role of several cytokines and adhesion molecules in reperfusion injury of the brain has been explored to a certain extent, their regulatory and temporary profiles remain unclear. We have addressed the temporal features of the induction of mRNA for proinflammatory cytokines, adhesion molecules and chemokines at an acute phase subsequent to reperfusion in rat forebrain. Semiquantitatively calibrated reverse transcription-polymerase chain reaction analysis was employed to assess the relative expression of mRNA for intercellular adhesion molecule (ICAM)-1, interleukin (IL)-1 alpha, IL-1 beta, 1L-2, 1L-6, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, monocyte-chemoattractant protein (MCP)-1, and macrophage migration inhibitory factor (MIF). The increase in mRNA from the basal levels after reperfusion followed one of two different patterns; an increase occurring as early as 1 h, or a slight increase continuing up to 24 h after reperfusion. The former pattern was seen for ICAM-1, IL-1 alpha, IL-1 beta, TNF-alpha, and MCP-1, and the latter for IL-6 and MIF. These results were consistent with the proinflammatory properties of the immediately induced cytokines, which may be involved in the initiation step of the inflammatory cascade, causing the secondary cellular responses and finally leading to further brain damage.