Acute inflammation plays an important role in host tissue defense against injury and infection, and also subsequent tissue repair. In the central nervous system parenchyma, following many types of insults, the acute inflammatory response to rapid neuronal degeneration or challenge with inflammatory substances differs dramatically from that of other tissues. The rapid recruitment of neutrophils is virtually absent and monocytes are only recruited after a delay of several days. It appears that the microenvironment of the central nervous system has evolved mechanisms to protect it from the potentially damaging consequences of some aspects of the acute inflammatory response.

Redness, heat, swelling and pain, the four cardinal signs of an acute inflammatory response in skin would appear to be of little relevance when thinking about the response to injury, cell degeneration or irdection in the central and peripheral nervous systems (CNS and PNS). However, one way to think of the acute inflammatory response is that it is the body's means of delivering circulating neutrophils and monocytes, which are the precursors of macrophages, to a site of infection or injury. These professional phagocytes then function at the site of injury to kill invading microorganisms, remove the debris, and facilitate tissue repair and the return to homeostasis. There is evidence that macrophages play a part in tissue repair after injury 1'2. In addition, their delivery is associated with activation of platelets and plasma protein cascades (coagulation, complement, kinin generation), increased expression of adhesion molecules on the vasculature and increases in vascular permeability.