The duality of the inflammatory response to traumatic brain injury |
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Authors: | Philipp M Lenzlinger Maria-Cristina Morganti-Kossmann Helmut L Laurer Tracy K McIntosh |
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Institution: | (1) Department of Neurosurgery, University of Pennsylvania, and Veterans Administration Medical Center, 105 Hayden Hall, 3320 Smith Walk, 19104-6316 Philadelphia, PA, USA;(2) Division of Trauma Surgery, University Hospital, Raemistrasse 100, CH-8091 Zurich, Switzerland |
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Abstract: | One and a half to two million people sustain a traumatic brain injury (TBI) in the US each year, of which approx 70,000–90,000
will suffer from long-term disability with dramatic impacts on their own and their families’ lives and enormous socio-economic
costs. Brain damage following traumatic injury is a result of direct (immediate mechanical disruption of brain tissue, or
primary injury) and indirect (secondary or delayed) mechanisms. These secondary mechanisms involve the initiation of an acute
inflammatory response, including breakdown of the blood-brain barrier (BBB), edema formation and swelling, infiltration of
peripheral blood cells and activation of resident immunocompetent cells, as well as the intrathecal release of numerous immune
mediators such as interleukins and chemotactic factors. An overview over the inflammatory response to trauma as observed in
clinical and in experimental TBI is presented in this review. The possibly harmful/beneficial sequelae of post-traumatic inflammation
in the central nervous system (CNS) are discussed using three model mediators of inflammation in the brain, tumor necrosis
factor-α (TNF-α), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β). While the former two may act as important
mediators for the initiation and the support of post-traumatic inflammation, thus causing additional cell death and neurologic
dysfunction, they may also pave the way for reparative processes. TGF-β, on the other hand, is a potent anti-inflammatory
agent, which may also have some deleterious long-term effects in the injured brain. The implications of this duality of the
post-traumatic inflammatory response for the treatment of brain-injured patients using anti-inflammatory strategies are discussed. |
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Keywords: | Traumatic brain injury inflammation neurons astrocytes microglia blood brain barrier cytokines interleukin-6 transforming growth factor-β tumor necrosis factor-α |
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