Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Mammalian neurones of the central nervous system (CNS) are terminally differentiated, and there is little endogenous capacity of the CNS to repair itself. Peripheral tissue injury, disease or infection results in a stereotypical inflammatory response to protect the host from pathogens and to promote tissue repair. However, collateral or 'bystander' damage is characteristic of any inflammatory response. Thus, it is apparent that the CNS has evolved mechanisms to regulate tightly the acute inflammatory response, and in particular to restrict the recruitment of neutrophils, in an attempt to protect itself from the potentially damaging consequences of inflammation in the brain. However, neutrophils are not always excluded from the brain. Indeed, they are found in large numbers in the brain parenchyma following traumatic lesions, stroke lesions, and in rodents, during the 'window of susceptibility'. Therapy targeted at blocking excitotoxic cell death has not successfully transferred from rodent models of stroke to human stroke patients. Restricting leukocyte entry to the brain, thereby inhibiting the inflammatory response, may prove to be a more practical therapeutic approach. The evidence presented in this review suggests that antagonising the effects of CXC chemokines may represent one route to achieve this goal.

Original publication

DOI

10.1517/13543784.8.4.363

Type

Journal article

Journal

Expert Opin Investig Drugs

Publication Date

04/1999

Volume

8

Pages

363 - 371