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, IL-1ß, IL-6, and TNF- Impart Neuroprotection to an Excitotoxin Through Distinct Pathways1
,§,
*
Geriatric Research Education and Clinical Center, Veterans Administration Medical Center, Salt Lake City, UT 84112;
Human Molecular Biology and Genetics Program, and Departments of
Internal Medicine and
§
Neurobiology and Anatomy, University of Utah, Salt Lake City, UT 84112
The proinflammatory cytokines IL-1
, IL-1ß, IL-6, and TNF-
are produced within the CNS, and, similar to the periphery, they have
pleotrophic and overlapping functions. We have shown previously that
TNF- increases neuronal survival to a toxic influx of calcium
mediated through neuronal
N-methyl-D-aspartic acid (NMDA)
glutamate-gated ion channels. This process, termed excitotoxicity, is a
major contributor to neuronal death following ischemia or stroke.
Neuroprotection by this cytokine requires both activation of the
p55/TNF receptor type I and the release of TNF- from neurons, and it
is inhibited by the plant alkaloid nicotine. Here, we report that other
inflammatory cytokines (IL-1, IL-1ß, and IL-6) are also
neuroprotective to excessive NMDA challenge in our system.
Neuroprotection provided by IL-1 is distinct from TNF- because it is
inhibited by IL-1 receptor antagonist; it is not antagonized by
nicotine, but it is inhibited by a neutralizing Ab to nerve growth
factor (NGF). Similar to IL-1, IL-6-mediated neuroprotection is also
antagonized by pretreatment with IL-1 receptor antagonist and it is not
affected by nicotine. However, neutralizing anti-NGF only partially
blocks IL-6-mediated protection. These studies support an important
role for distinct but overlapping neuroprotective cytokine effects in
the CNS.
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