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Contributions of the immune system to the pathophysiology of traumatic brain injury - evidence by intravital microscopy.

Schwarzmaier SM, Plesnila N - Front Cell Neurosci (2014)

Bottom Line: Traumatic brain injury (TBI) results in immediate brain damage that is caused by the mechanical impact and is non-reversible.Among these secondary mechanisms, the inflammatory response is believed to play an important role, mediating actions that can have both protective and detrimental effects on the progression of secondary brain damage.Histological data generated extensive information; however, this is only a snapshot of processes that are, in fact, very dynamic.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, University of Munich Medical Center Munich, Germany ; Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center Munich, Germany.

ABSTRACT
Traumatic brain injury (TBI) results in immediate brain damage that is caused by the mechanical impact and is non-reversible. This initiates a cascade of delayed processes which cause additional-secondary-brain damage. Among these secondary mechanisms, the inflammatory response is believed to play an important role, mediating actions that can have both protective and detrimental effects on the progression of secondary brain damage. Histological data generated extensive information; however, this is only a snapshot of processes that are, in fact, very dynamic. In contrast, in vivo microscopy provides detailed insight into the temporal and spatial patterns of cellular dynamics. In this review, we aim to summarize data which was generated by in vivo microscopy, specifically investigating the immune response following brain trauma, and its potential effects on secondary brain damage.

No MeSH data available.


Related in: MedlinePlus

Scheme of pathophysiological reactions of leukocytes and microglia after traumatic brain injury as demonstrated by in vivo experiments. Under physiological conditions (green background), leukocytes pass the cerebral microcirculation in undisturbed blood flow, while some of them occasionally role on the endothelium. Microglia have a ramified shape and continuously scan the brain parenchyma with their processes. Following TBI (red background), the intravascular leukocytes start rolling and adhering to the endothelium, mediated by selectins and integrins respectively. Finally, they migrate into the damaged tissue. Microglia become activated by brain trauma, extend their processes towards the site of injury, and finally migrate towards the injury, taking up an amoeboid shape.
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Figure 1: Scheme of pathophysiological reactions of leukocytes and microglia after traumatic brain injury as demonstrated by in vivo experiments. Under physiological conditions (green background), leukocytes pass the cerebral microcirculation in undisturbed blood flow, while some of them occasionally role on the endothelium. Microglia have a ramified shape and continuously scan the brain parenchyma with their processes. Following TBI (red background), the intravascular leukocytes start rolling and adhering to the endothelium, mediated by selectins and integrins respectively. Finally, they migrate into the damaged tissue. Microglia become activated by brain trauma, extend their processes towards the site of injury, and finally migrate towards the injury, taking up an amoeboid shape.

Mentions: Following brain injury, microglia extend their processes towards the damaged area as shown in vivo after laser or microelectrode injury (Davalos et al., 2005), or ex vivo on organotropic hippocampal slice cultures following MCAo (Neumann et al., 2008; Figure 1). Microglia morphologically become more amoeboid and finally migrate towards the site of injury (Kim and Dustin, 2006). These changes in morphology and/or migration resulted in encapsulation of the damaged area (Davalos et al., 2005; Kim and Dustin, 2006), or in engulfment of invading neutrophils (Neumann et al., 2008). The laser injury was performed by high laser power delivered to a dedicated area of interest for a certain time, and the microelectrode injury was induced with a glass electrode which was inserted into the cortex by a micromanipulator (Davalos et al., 2005). Both laser injury and microelectrode injury result in a very small, focal brain damage. Consequently, these techniques provide excellent models for studying very subtle alterations of cells or even subcellular processes in a well-defined area. While these studies generate valuable information on microglia and their functions, they do not mimic clinical brain injury. The dynamics of a TBI, however, can cause a much stronger and more complex damage—depending on injury severity and mechanism—which might affect or activate the resident immune cells quite differently.


Contributions of the immune system to the pathophysiology of traumatic brain injury - evidence by intravital microscopy.

Schwarzmaier SM, Plesnila N - Front Cell Neurosci (2014)

Scheme of pathophysiological reactions of leukocytes and microglia after traumatic brain injury as demonstrated by in vivo experiments. Under physiological conditions (green background), leukocytes pass the cerebral microcirculation in undisturbed blood flow, while some of them occasionally role on the endothelium. Microglia have a ramified shape and continuously scan the brain parenchyma with their processes. Following TBI (red background), the intravascular leukocytes start rolling and adhering to the endothelium, mediated by selectins and integrins respectively. Finally, they migrate into the damaged tissue. Microglia become activated by brain trauma, extend their processes towards the site of injury, and finally migrate towards the injury, taking up an amoeboid shape.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4219391&req=5

Figure 1: Scheme of pathophysiological reactions of leukocytes and microglia after traumatic brain injury as demonstrated by in vivo experiments. Under physiological conditions (green background), leukocytes pass the cerebral microcirculation in undisturbed blood flow, while some of them occasionally role on the endothelium. Microglia have a ramified shape and continuously scan the brain parenchyma with their processes. Following TBI (red background), the intravascular leukocytes start rolling and adhering to the endothelium, mediated by selectins and integrins respectively. Finally, they migrate into the damaged tissue. Microglia become activated by brain trauma, extend their processes towards the site of injury, and finally migrate towards the injury, taking up an amoeboid shape.
Mentions: Following brain injury, microglia extend their processes towards the damaged area as shown in vivo after laser or microelectrode injury (Davalos et al., 2005), or ex vivo on organotropic hippocampal slice cultures following MCAo (Neumann et al., 2008; Figure 1). Microglia morphologically become more amoeboid and finally migrate towards the site of injury (Kim and Dustin, 2006). These changes in morphology and/or migration resulted in encapsulation of the damaged area (Davalos et al., 2005; Kim and Dustin, 2006), or in engulfment of invading neutrophils (Neumann et al., 2008). The laser injury was performed by high laser power delivered to a dedicated area of interest for a certain time, and the microelectrode injury was induced with a glass electrode which was inserted into the cortex by a micromanipulator (Davalos et al., 2005). Both laser injury and microelectrode injury result in a very small, focal brain damage. Consequently, these techniques provide excellent models for studying very subtle alterations of cells or even subcellular processes in a well-defined area. While these studies generate valuable information on microglia and their functions, they do not mimic clinical brain injury. The dynamics of a TBI, however, can cause a much stronger and more complex damage—depending on injury severity and mechanism—which might affect or activate the resident immune cells quite differently.

Bottom Line: Traumatic brain injury (TBI) results in immediate brain damage that is caused by the mechanical impact and is non-reversible.Among these secondary mechanisms, the inflammatory response is believed to play an important role, mediating actions that can have both protective and detrimental effects on the progression of secondary brain damage.Histological data generated extensive information; however, this is only a snapshot of processes that are, in fact, very dynamic.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, University of Munich Medical Center Munich, Germany ; Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center Munich, Germany.

ABSTRACT
Traumatic brain injury (TBI) results in immediate brain damage that is caused by the mechanical impact and is non-reversible. This initiates a cascade of delayed processes which cause additional-secondary-brain damage. Among these secondary mechanisms, the inflammatory response is believed to play an important role, mediating actions that can have both protective and detrimental effects on the progression of secondary brain damage. Histological data generated extensive information; however, this is only a snapshot of processes that are, in fact, very dynamic. In contrast, in vivo microscopy provides detailed insight into the temporal and spatial patterns of cellular dynamics. In this review, we aim to summarize data which was generated by in vivo microscopy, specifically investigating the immune response following brain trauma, and its potential effects on secondary brain damage.

No MeSH data available.


Related in: MedlinePlus