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New perspectives on central and peripheral immune responses to acute traumatic brain injury.

Das M, Mohapatra S, Mohapatra SS - J Neuroinflammation (2012)

Bottom Line: TBI disrupts the blood-brain barrier (BBB) leading to infiltration of immune cells into the brain and subsequent inflammation and neurodegeneration.TBI-induced peripheral immune responses can also result in multiorgan damage.Despite worldwide research efforts, the methods of diagnosis, monitoring and treatment for TBI are still relatively ineffective.

View Article: PubMed Central - HTML - PubMed

Affiliation: Nanomedicine Research Center, University of South Florida Morsani College of Medicine, 12901 Bruce B. Downs Blvd., Tampa, FL 33612, USA.

ABSTRACT
Traumatic injury to the brain (TBI) results in a complex set of responses involving various symptoms and long-term consequences. TBI of any form can cause cognitive, behavioral and immunologic changes in later life, which underscores the problem of underdiagnosis of mild TBI that can cause long-term neurological deficits. TBI disrupts the blood-brain barrier (BBB) leading to infiltration of immune cells into the brain and subsequent inflammation and neurodegeneration. TBI-induced peripheral immune responses can also result in multiorgan damage. Despite worldwide research efforts, the methods of diagnosis, monitoring and treatment for TBI are still relatively ineffective. In this review, we delve into the mechanism of how TBI-induced central and peripheral immune responses affect the disease outcome and discuss recent developments in the continuing effort to combat the consequences of TBI and new ways to enhance repair of the damaged brain.

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Possible mechanism and the interactions between brain and systemic immunity after traumatic brain injury (TBI). Blood–brain barrier (BBB) disruption allows peripheral immune cell infiltration into the brain. Interaction between brain and peripheral immune organs can cause either hyperinflammation or immune suppression. Anti-inflammatory cytokines may eventually lead to neuronal recovery.
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Figure 1: Possible mechanism and the interactions between brain and systemic immunity after traumatic brain injury (TBI). Blood–brain barrier (BBB) disruption allows peripheral immune cell infiltration into the brain. Interaction between brain and peripheral immune organs can cause either hyperinflammation or immune suppression. Anti-inflammatory cytokines may eventually lead to neuronal recovery.

Mentions: Once the brain suffers mechanical insult, the injury process evolves over time and includes (a) primary injury caused by direct or indirect contusion resulting in shearing or stretching of brain tissue, subdural hematoma and cerebral ischemia (b) secondary injury characterized by diffuse axonal injury and inflammatory reactions, and (c) regeneration. The secondary, that is, the nonmechanical injury phase, is progressive and lasts from hours to days[13,14], significantly contributing to neurological disabilities[15]. Injury to the cerebral vasculature breaks the blood–brain barrier (BBB), allows entry of immune cells and stimulates inflammatory reactions. The molecular events result in apoptosis, inflammation, altered plasticity and neuronal regeneration. The complex nature of acute and chronic inflammatory reactions may aggravate the pathologic outcome or promote the repair process[16,17]. Also, multiorgan damage in trauma patients can lead to elevated circulatory levels of inflammatory cytokines that may contribute to the post-TBI pathogenesis of the brain[18] and cause multiple organ dysfunction syndrome (MODS) and death[19]. In this review we discuss the mechanism of interaction between the systemic immune response and the brain after TBI and current novel treatment approaches to combat TBI-induced damage (Figure1).


New perspectives on central and peripheral immune responses to acute traumatic brain injury.

Das M, Mohapatra S, Mohapatra SS - J Neuroinflammation (2012)

Possible mechanism and the interactions between brain and systemic immunity after traumatic brain injury (TBI). Blood–brain barrier (BBB) disruption allows peripheral immune cell infiltration into the brain. Interaction between brain and peripheral immune organs can cause either hyperinflammation or immune suppression. Anti-inflammatory cytokines may eventually lead to neuronal recovery.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3526406&req=5

Figure 1: Possible mechanism and the interactions between brain and systemic immunity after traumatic brain injury (TBI). Blood–brain barrier (BBB) disruption allows peripheral immune cell infiltration into the brain. Interaction between brain and peripheral immune organs can cause either hyperinflammation or immune suppression. Anti-inflammatory cytokines may eventually lead to neuronal recovery.
Mentions: Once the brain suffers mechanical insult, the injury process evolves over time and includes (a) primary injury caused by direct or indirect contusion resulting in shearing or stretching of brain tissue, subdural hematoma and cerebral ischemia (b) secondary injury characterized by diffuse axonal injury and inflammatory reactions, and (c) regeneration. The secondary, that is, the nonmechanical injury phase, is progressive and lasts from hours to days[13,14], significantly contributing to neurological disabilities[15]. Injury to the cerebral vasculature breaks the blood–brain barrier (BBB), allows entry of immune cells and stimulates inflammatory reactions. The molecular events result in apoptosis, inflammation, altered plasticity and neuronal regeneration. The complex nature of acute and chronic inflammatory reactions may aggravate the pathologic outcome or promote the repair process[16,17]. Also, multiorgan damage in trauma patients can lead to elevated circulatory levels of inflammatory cytokines that may contribute to the post-TBI pathogenesis of the brain[18] and cause multiple organ dysfunction syndrome (MODS) and death[19]. In this review we discuss the mechanism of interaction between the systemic immune response and the brain after TBI and current novel treatment approaches to combat TBI-induced damage (Figure1).

Bottom Line: TBI disrupts the blood-brain barrier (BBB) leading to infiltration of immune cells into the brain and subsequent inflammation and neurodegeneration.TBI-induced peripheral immune responses can also result in multiorgan damage.Despite worldwide research efforts, the methods of diagnosis, monitoring and treatment for TBI are still relatively ineffective.

View Article: PubMed Central - HTML - PubMed

Affiliation: Nanomedicine Research Center, University of South Florida Morsani College of Medicine, 12901 Bruce B. Downs Blvd., Tampa, FL 33612, USA.

ABSTRACT
Traumatic injury to the brain (TBI) results in a complex set of responses involving various symptoms and long-term consequences. TBI of any form can cause cognitive, behavioral and immunologic changes in later life, which underscores the problem of underdiagnosis of mild TBI that can cause long-term neurological deficits. TBI disrupts the blood-brain barrier (BBB) leading to infiltration of immune cells into the brain and subsequent inflammation and neurodegeneration. TBI-induced peripheral immune responses can also result in multiorgan damage. Despite worldwide research efforts, the methods of diagnosis, monitoring and treatment for TBI are still relatively ineffective. In this review, we delve into the mechanism of how TBI-induced central and peripheral immune responses affect the disease outcome and discuss recent developments in the continuing effort to combat the consequences of TBI and new ways to enhance repair of the damaged brain.

Show MeSH
Related in: MedlinePlus