Neuroinflammation: the devil is in the details

Journal of Neurochemistry, Год журнала: 2016, Номер 139(S2), С. 136 - 153

Опубликована: Март 19, 2016

Abstract There is significant interest in understanding inflammatory responses within the brain and spinal cord. Inflammatory that are centralized cord generally referred to as ‘neuroinflammatory’. Aspects of neuroinflammation vary context disease, injury, infection, or stress. The context, course, duration these all critical aspects processes their corresponding physiological, biochemical, behavioral consequences. Microglia, innate immune cells CNS , play key roles mediating neuroinflammatory responses. Because connotation inherently negative maladaptive, majority research focus on pathological neuroinflammation. are, however, several degrees responses, some which positive. In many circumstances including there a balance intrinsic repair influences functional recovery. addition, other examples where communication between system involves beneficial adaptive. purpose this review distinguish different variations context‐specific manner detail both positive processes. image review, we will use stress, aging, events illustrate potential harm benefits inherent Context, inflammation highly important interpretation events, aim provide insight into by detailing commonly studied insults. This article part 60th anniversary supplemental issue .

Язык: Английский

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The far-reaching scope of neuroinflammation after traumatic brain injury

Nature Reviews Neurology, Год журнала: 2017, Номер 13(3), С. 171 - 191

Опубликована: Фев. 10, 2017

Язык: Английский

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Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift

Neuron, Год журнала: 2017, Номер 95(6), С. 1246 - 1265

Опубликована: Сен. 1, 2017

Язык: Английский

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The role of inflammation in the development of epilepsy

Journal of Neuroinflammation, Год журнала: 2018, Номер 15(1)

Опубликована: Май 15, 2018

Epilepsy, a neurological disease characterized by recurrent seizures, is often associated with history of previous lesions in the nervous system. Impaired regulation activation and resolution inflammatory cells molecules injured neuronal tissue critical factor to development epilepsy. However, it still unclear as how that unbalanced inflammation contributes Therefore, one goals epilepsy research identify elucidate interconnected pathways systemic disorders may further develop progression. In this paper, molecules, (rheumatoid arthritis, Crohn’s, Type I Diabetes, etc.) could contribute development, are reviewed. Understanding neurobiology epileptogenesis will new biomarkers for better screening patients at risk therapeutic targets both prophylaxis treatment

Язык: Английский

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Inflammation: the link between comorbidities, genetics, and Alzheimer’s disease

Journal of Neuroinflammation, Год журнала: 2018, Номер 15(1)

Опубликована: Сен. 24, 2018

Alzheimer’s disease (AD) is a neurodegenerative disorder, most cases of which lack clear causative event. This has made the difficult to characterize and, thus, diagnose. Although some are genetically linked, there many diseases and lifestyle factors that can lead an increased risk developing AD, including traumatic brain injury, diabetes, hypertension, obesity, other metabolic syndromes, in addition aging. Identifying common trends between these conditions could enhance our understanding AD development more effective treatments. immune system one body’s key defense mechanisms, chronic inflammation been increasingly linked with several age-related diseases. Moreover, it now well accepted important role onset progression AD. In this review, different inflammatory signals associated its will be outlined demonstrate how may influencing individual susceptibility Our goal bring attention potential shared presented by during successful

Язык: Английский

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Distinct Contributions of Astrocytes and Pericytes to Neuroinflammation Identified in a 3D Human Blood-Brain Barrier on a Chip

PLoS ONE, Год журнала: 2016, Номер 11(3), С. e0150360 - e0150360

Опубликована: Март 1, 2016

Neurovascular inflammation is a major contributor to many neurological disorders, but modeling these processes in vitro has proven be difficult. Here, we microengineered three-dimensional (3D) model of the human blood-brain barrier (BBB) within microfluidic chip by creating cylindrical collagen gel containing central hollow lumen inside microchannel, culturing primary brain microvascular endothelial cells on gel's inner surface, and flowing medium through lumen. Studies were carried out with engineered microvessel endothelium presence or absence either pericytes beneath astrocytes surrounding explore ability this simplified identify distinct contributions supporting neuroinflammatory response. This 3D BBB-on-a-chip exhibited permeability similar that observed other BBB models created non-human cells, when stimulated inflammatory trigger, tumor necrosis factor-alpha (TNF-α), different secretion profiles for granulocyte colony-stimulating factor (G-CSF) interleukin-6 (IL-6) depending pericytes. Importantly, levels responses detected significantly greater than same co-cultured static Transwell plates. Thus, as G-CSF IL-6 have been reported play important roles neuroprotection neuroactivation vivo, potentially offers new method study neurovascular function vitro, physiological individual cell types.

Язык: Английский

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Severe traumatic brain injury: targeted management in the intensive care unit

The Lancet Neurology, Год журнала: 2017, Номер 16(6), С. 452 - 464

Опубликована: Май 10, 2017

Язык: Английский

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Inflammatory neuroprotection following traumatic brain injury

Science, Год журнала: 2016, Номер 353(6301), С. 783 - 785

Опубликована: Авг. 18, 2016

Traumatic brain injury (TBI) elicits an inflammatory response in the central nervous system (CNS) that involves both resident and peripheral immune cells. Neuroinflammation can persist for years following a single TBI may contribute to neurodegeneration. However, administration of anti-inflammatory drugs shortly after was not effective treatment patients. Some components neuroinflammatory seem play beneficial role acute phase TBI. Indeed, CNS injury, early inflammation set stage proper tissue regeneration recovery, which can, perhaps, explain why general immunosuppression patients is disadvantageous. Here, we discuss some positive attributes neuroinflammation propose be therapeutically guided rather than globally suppressed.

Язык: Английский

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Traumatic Axonal Injury: Mechanisms and Translational Opportunities

Trends in Neurosciences, Год журнала: 2016, Номер 39(5), С. 311 - 324

Опубликована: Апрель 2, 2016

Язык: Английский

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Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation

Journal of Neuroinflammation, Год журнала: 2016, Номер 13(1)

Опубликована: Окт. 11, 2016

The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary factor that can drive ongoing neuronal injury. Despite this, treatments have targeted aspects of the inflammatory pathway not shown significant efficacy in clinical trials. We suggest this may because classical inflammation only represents part story, with activation neurogenic potentially one initiating events TBI. Indeed, evidence suggests transient receptor potential cation channels (TRP channels), TRPV1 and TRPA1, are polymodal receptors activated by variety stimuli associated TBI, including mechanical shear stress, leading release neuropeptides such as substance P (SP). SP augments many via microglia astrocytes, degranulation mast cells, promoting leukocyte migration. Furthermore, initiate earliest changes seen blood-brain barrier (BBB) permeability, namely increased transcellular transport plasma proteins caveolae. This line reports alterations first prior decreases expression tight-junction claudin-5 occludin. for SP, tachykinin NK1 receptor, found caveolae its TBI allow influx albumin other which directly augment activating astrocytes microglia. As such, exacerbate positive feedback loop, mediators bradykinin prostaglandins then further stimulating TRP receptors. Accordingly, complete inhibition neuroinflammation require both pathways.

Язык: Английский

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