الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
An acute inflammatory response in the CNS is caused by the immediate and early
activation of the glial cell in response to toxic stimuli, which is basically a defensive
response that leads to repair of the damaged area. But, if the “stimulus” remains persistent
in time, an inflammatory condition develops, causing a phenomenon of cumulative damage
over time due to the chronic inflammatory reaction. All these events precede and cause
neuronal degeneration, generating complex interactions and feedback loops between glial
and neuronal cells, leading to cell damage and to the development of a neurodegenerative
disease. Thus, neuroinflammation has beneficial or deleterious results in the brain mainly
depending on the duration of the inflammatory response.
Lipopolysaccharide (LPS) the most abundant component within the cell wall of
Gram-negative bacteria can stimulate the release of different inflammatory cytokines in
various cell types, leading to an acute inflammatory response to the brain. In the present
study, we evaluated how systemic inflammation induced by intraperitoneal injection (ip) of
lipopolysaccharides (LPS) affected brain inflammation and neuronal damage in the rat.
The results of the present study show that ip LPS injection indeed induced brain
inflammation. Microglia became morphologically activated; neutrophils infiltrated the
brain; and inflammatory mediators, including interleukin-1β (IL-1β), tumor necrosis-alpha
(TNF-α), IL-6, and iNOS were synthesized. However, no neuronal death was evident.
These results indicate that systemic inflammation indeed causes brain inflammation, but to
only a mild extent and does not result in neuronal death