Traumatic Brain Injury and Inflammation: Emerging Role of Innate and Adaptive Immunity

Dardiotis, Efthimios; Karanikas, Vaios; Paterakis, Konstantinos; Fountas, Kostas N.; Hadjigeorgiou, Georgios M.

doi:10.5772/27840

Cited by 17 publications

(18 citation statements)

References 125 publications

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“…Head trauma initially triggers inflammation by a variety of factors including direct damage to the BBB as well as an accumulation of foreign particles, extravasated blood proteins, cellular debris, complement fragments, prostaglandins, and both reactive oxygen and nitrogen species within the brain (Dardiotis et al, 2012). The resulting inflammatory cascade involves the coordinated activity of resident central nervous system (CNS) immune and non-immune cells, circulating immune cells, and transport mechanisms across the BBB.…”

Section: Brain Inflammation and Blood–brain Barrier Dysfunction Aftermentioning

confidence: 99%

“…The invasion of leukocytes (chiefly neutrophils, monocytes, and lymphocytes) results in further disruption of homeostasis and secretion of pro-inflammatory signals within acutely spared brain regions resulting in a potent inflammatory response to these sites (Morganti-Kossmann et al, 2001). Additional increases in BBB permeability magnify levels of inflammatory units and blood proteins entering brain tissue (Dardiotis et al, 2012). …”

Section: Brain Inflammation and Blood–brain Barrier Dysfunction Aftermentioning

confidence: 99%

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Neural circuit mechanisms of post–traumatic epilepsy

Hunt¹,

Boychuk²,

Smith³

2013

Front. Cell. Neurosci.

142

134

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Traumatic brain injury (TBI) greatly increases the risk for a number of mental health problems and is one of the most common causes of medically intractable epilepsy in humans. Several models of TBI have been developed to investigate the relationship between trauma, seizures, and epilepsy-related changes in neural circuit function. These studies have shown that the brain initiates immediate neuronal and glial responses following an injury, usually leading to significant cell loss in areas of the injured brain. Over time, long-term changes in the organization of neural circuits, particularly in neocortex and hippocampus, lead to an imbalance between excitatory and inhibitory neurotransmission and increased risk for spontaneous seizures. These include alterations to inhibitory interneurons and formation of new, excessive recurrent excitatory synaptic connectivity. Here, we review in vivo models of TBI as well as key cellular mechanisms of synaptic reorganization associated with post-traumatic epilepsy (PTE). The potential role of inflammation and increased blood–brain barrier permeability in the pathophysiology of PTE is also discussed. A better understanding of mechanisms that promote the generation of epileptic activity versus those that promote compensatory brain repair and functional recovery should aid development of successful new therapies for PTE.

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Section: Brain Inflammation and Blood–brain Barrier Dysfunction Aftermentioning

confidence: 99%

Section: Brain Inflammation and Blood–brain Barrier Dysfunction Aftermentioning

confidence: 99%

Neural circuit mechanisms of post–traumatic epilepsy

Hunt¹,

Boychuk²,

Smith³

2013

Front. Cell. Neurosci.

142

134

View full text Add to dashboard Cite

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“…Although the brain has long been considered immunologically privileged, new evidence suggests that the intrinsic immuno-regulatory properties of central nervous system (CNS) cells, as well as peripheral immune cells and molecules crossing the blood-brain barrier (BBB), influence the brain’s response to injury (Becher et al, 2000; Dardiotis et al, 2012). Additionally, cytokine trafficking may occur via receptor-mediated transcytosis or activation of afferent vagal fibers (Banks, 2005; Maier et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Variable neuroendocrine–immune dysfunction in individuals with unfavorable outcome after severe traumatic brain injury

Santarsieri

Kumar

Kochanek

et al. 2015

Brain, Behavior, and Immunity

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Bidirectional communication between the immune and neuroendocrine systems is not well understood in the context of traumatic brain injury (TBI). The purpose of this study was to characterize relationships between cerebrospinal fluid (CSF) cortisol and inflammation after TBI, and to determine how these relationships differ by outcome. CSF samples were collected from 91 subjects with severe TBI during days 0–6 post-injury, analyzed for cortisol and inflammatory markers, and compared to healthy controls (n=13 cortisol, n=11 inflammatory markers). Group-based trajectory analysis (TRAJ) delineated subpopulations with similar longitudinal CSF cortisol profiles (high vs. low cortisol). Glasgow Outcome Scale (GOS) scores at 6 months served as the primary outcome measure reflecting global outcome. Inflammatory markers that displayed significant bivariate associations with both GOS and cortisol TRAJ (interleukin [IL]-6, IL-10, soluble Fas [sFas], soluble intracellular adhesion molecule [sICAM]-1, and tumor necrosis factor alpha [TNF]-α) were used to generate a cumulative inflammatory load score (ILS). Subsequent analysis revealed that cortisol TRAJ group membership mediated ILS effects on outcome (indirect effect estimate= −0.253, 95% CI (−0.481, −0.025), p=0.03). Correlational analysis between mean cortisol levels and ILS were examined separately within each cortisol TRAJ group and by outcome. Within the low cortisol TRAJ group, subjects with unfavorable 6-month outcome displayed a negative correlation between ILS and mean cortisol (r=−0.562, p=0.045). Conversely, subjects with unfavorable outcome in the high cortisol TRAJ group displayed a positive correlation between ILS and mean cortisol (r=0.391, p=0.006). Our results suggest that unfavorable outcome after TBI may result from dysfunctional neuroendocrine-immune communication wherein an adequate immune response is not mounted or, alternatively, neuroinflammation is prolonged. Importantly, the nature of neuroendocrine-immune dysfunction differs between cortisol TRAJ groups. These results present a novel biomarker-based index from which to discriminate outcome and emphasize the need for evaluating tailored treatments targeting inflammation early after injury.

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“…Secondary injuries are slow to change and may be a major factor in the patient's recovery [1]. Primary damage to the brain and central nervous system occurs with the initial insult (lacerations, fracture, contusions, axonal injury, intracranial hemorrhage), whereas a secondary injury is the resultant of such factors as increased intracranial pressure, interruption in the brain blood barrier flow, brain inflammation, disruptions in cerebral blood flow, ischemia, hypoxia, reperfusion, and/or reoxygenation injury [8,9]. In addition, a series of events can lead to an accumulation of white blood cells in the injured brain area can lead to inflammation and secondary brain damage.…”

Section: Brain Injuriesmentioning

confidence: 99%

“…Brain injuries can be classified according to several dichotomous taxonomies, that is, primary vs. secondary injuries, focal vs. diffuse pathologies, and inflammatory vs. non-inflammatory diseases [7][8][9]. Traumatic brain injuries (TBIs) s can be classified into two categories of primary and secondary injuries [1].…”

Section: Brain Injuriesmentioning

confidence: 99%

Recovery from Diffuse Brain Injuries: Two Case Studies

Brice¹,

Brice²

2017

Advances in Speech-Language Pathology

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Subarachnoid hemorrhages (SAHs) are grave medical emergencies, whereas 30-50% of all SAHs may ultimately result in death. Subarachnoid hemorrhages share many resemblances with other neurological traumas such as a cerebral vascular accident, meningitis, and/or traumatic brain injury. Autoimmune encephalopathies (AE) occur when human antibodies assault the body's cell surfaces and/or synaptic proteins. Consequently, widespread nervous system and diffuse brain involvement may occur.With subarachnoid hemorrhages and autoimmune encephalopathies, multiple areas of cognition and language can be impaired. Case studies in communication sciences and disorders are underutilized, yet are important in evidenced-based practice. Speechlanguage pathologists in medical settings have worked with patients and families with similar types of disorders. Therefore, speech-language pathologists should be well equipped to provide therapy with these types of injuries. This chapter presents two case studies and cognitive language rehabilitation strategies following diffuse brain injuries.

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Traumatic Brain Injury and Inflammation: Emerging Role of Innate and Adaptive Immunity

Cited by 17 publications

References 125 publications

Neural circuit mechanisms of post–traumatic epilepsy

Neural circuit mechanisms of post–traumatic epilepsy

Variable neuroendocrine–immune dysfunction in individuals with unfavorable outcome after severe traumatic brain injury

Recovery from Diffuse Brain Injuries: Two Case Studies

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