Reducing Neuroinflammation

Abstract

The response of living tissue to injury is characterized by an increase in blood flow and a local influx of leukocytes. These events, mediated by either the upregulation or induction of adhesion molecules and the release of biologically active substances, are collectively termed inflammation. The inflammatory response is not antigen-specific and occurs following all modes of tissue injury, including traumatic, ischemic, and infectious insults. In infection, the inflammatory response is usually accompanied by an immune response, which is antigen specific. The brain has traditionally been regarded as an immunologically privileged organ, but it is subject to continuous lymphocyte surveillance and inflammatory and immunological reactions do occur in the brain. The character of the inflammatory response in the brain, however, differs from that of other organs. These differences result from the fact that under normal circumstances, the blood-brain barrier (BBB) exists and the cerebral microvessels express few of the adhesion molecules required for leukocyte trafficking into the brain. But when the brain is injured, the BBB becomes compromised (Belayev et al. 1996) and there is an upregulation of leukocyte adhesion molecules, both of which allow for an inflammatory response, and potentially an immune response, to occur.