This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
There is increasing evidence that the inflammatory response plays an important role in the potentiation of central nervous system (CNS) ischemic injury. Much of this inflammatory response appears to be mediated by interleukins (IL), a multifunctional subclass of cytokines. The proinflammatory interleukins, including IL-1, tumor necrosis factor alpha(TNF-α), and IL-6, can influence the function and synthesis of other cytokines by a complex cytokine network.1 These proinflammatory interleukins are produced by a variety of cells, including microglial cells, astrocytes, and leukocytes, and appear to directly modulate CNS cell apoptosis, differentiation, and proliferation and to influence subsequent infiltration by leukocytes.1,2 Increased levels of IL-1, TNF-α, and IL-6 have been observed after experimental CNS ischemia.2,3 Indirect evidence for the involvement of interleukins in ischemic injury comes from several recent clinical studies which found that CSF and plasma levels of IL-6 predict the functional recovery of the patient and also correlate with the infarct size.4,5
The strongest support for the important role played by the inflammatory response in CNS ischemia comes from studies investigating the role of leukocyte adhesion and infiltration after stroke. A large number of studies have now shown that leukocytes adhere and infiltrate early after CNS ischemia and that agents that block leukocyte adhesion produce therapeutic benefits in a variety of animal models.6-8 Recent evidence suggests that cytokines may be key components in the activation and recruitment of leukocytes into the CNS. IL-1β, TNF-α, and IL-6 activate leukocytes and increase the expression of adhesion receptors on the leukocyte (CD-18) and on endothelial and astrocyte cells (intercellular adhesion molecule [ICAM]-1).2,9
The preceding evidence suggests that the inflammatory response is an important component of CNS ischemic injury and that the interleukins appear to play a key role in the modulation of this inflammatory response. By modulating the …
AAN Members
We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page.
AAN Non-Member Subscribers
Purchase access
Letters: Rapid online correspondence
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
