Controlled Cortical Impact and Craniotomy Induce Strikingly Similar Profiles of Inflammatory Gene Expression, but with Distinct Kinetics

Lagraoui, Mouna; Latoche, Joseph R.; Cartwright, Natalia G.; Sukumar, Gauthaman; Dalgard, Clifton L.; Schaefer, Brian C.

doi:10.3389/fneur.2012.00155

Cited by 87 publications

(85 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neuroinflammation as a result of endogenous immune activation in the brain is a universal response of the CNS to the injury aimed at limiting damage, restoring homeostasis, protecting neurons, and promoting tissue recovery and repair [18][19][20][21]. Activated by primary traumatic or non-traumatic brain injury, microglia produces several types of inflammatory mediators including LTA4 and LTB4 [37,38].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Zakharov

Kotikova

Nurieva

et al. 2017

Clinical Toxicology

View full text Add to dashboard Cite

Context: The role of neuroinflammation in methanol-induced toxic brain damage has not been studied. Objective: We studied acute concentrations and the dynamics of leukotrienes (LT) in serum in hospitalized patients with acute methanol poisoning and in survivors. Methods: Series of acute cysteinyl-LT and LTB4 concentration measurements were performed in 28/101 hospitalized patients (mean observation time: 88 ± 20 h). In 36 survivors, control LT measurements were performed 2 years after discharge. Results: The acute maximum (C max ) LT concentrations were higher than concentrations in survivors: C max for LTC4 was 80.7 ± 5.6 versus 47.9 ± 4.5 pg/mL; for LTD4, 51.0 ± 6.6 versus 23.1 ± 2.1 pg/mL; for LTE4, 64.2 ± 6.0 versus 26.2 ± 3.9 pg/mL; for LTB4, 59.8 ± 6.2 versus 27.2 ± 1.4 pg/mL (all p < 0.001). The patients who survived had higher LT concentrations than those who died (all p < 0.01). Among survivors, patients with CNS sequelae had lower LTE4 and LTB4 than did those without sequelae (both p < 0.05). The LT concentrations increased at a rate of 0.4-0.5 pg/mL/h and peaked 4-5 days after admission. The patients with better outcomes had higher cys-LTs (all p < 0.01) and LTB4 (p < 0.05). More severely poisoned patients had lower acute LT concentrations than those with minor acidemia. The follow-up LT concentrations in survivors with and without CNS sequelae did not differ (all p > 0.05). The mean decrease in LT concentration was 30.9 ± 9.0 pg/mL for LTC4, 26.3 ± 8.6 pg/mL for LTD4, 37.3 ± 6.4 pg/mL for LTE4, and 32.0 ± 8.8 pg/mL for LTB4. Conclusions: Our findings suggest that leukotriene-mediated neuroinflammation may play an important role in the mechanisms of toxic brain damage in acute methanol poisoning in humans. Acute elevation of LT concentrations was moderate, transitory, and was not followed by chronic neuroinflammation in survivors.ARTICLE HISTORY

show abstract

Section: Discussionmentioning

confidence: 99%

“…Neuroinflammation is one of the neuroprotective mechanisms associated with repair and recovery of the brain after acute traumatic and non-traumatic brain injury such as stroke, hypoxia, ischemia, and poisoning [18]. Leukotrienes (LTs) are the main mediators of neuroinflammation [19,20].…”

Section: Importancementioning

confidence: 99%

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Zakharov

Kotikova

Nurieva

et al. 2017

Clinical Toxicology

View full text Add to dashboard Cite

show abstract

“…Microarrays have previously been used to investigate gene expression in a range of different studies and have been extensively verified in mice and humans (Lagraoui et al, 2012;Trabzuni et al, 2011). After quality control steps, excluding probes or mice with insufficient signal (see Experimental Procedures), data were available for 12,588 genes and pathology in 113 hippocampus samples, 113 cortex samples, and 111 cerebellum samples.…”

Section: Introductionmentioning

confidence: 99%

A Genome-wide Gene-Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

et al. 2015

View full text Add to dashboard Cite

We provide microarray data comparing genome-wide differential expression and pathology throughout life in four lines of "amyloid" transgenic mice (mutant human APP, PSEN1, or APP/PSEN1) and "TAU" transgenic mice (mutant human MAPT gene). Microarray data were validated by qPCR and by comparison to human studies, including genome-wide association study (GWAS) hits. Immune gene expression correlated tightly with plaques whereas synaptic genes correlated negatively with neurofibrillary tangles. Network analysis of immune gene modules revealed six hub genes in hippocampus of amyloid mice, four in common with cortex. The hippocampal network in TAU mice was similar except that Trem2 had hub status only in amyloid mice. The cortical network of TAU mice was entirely different with more hub genes and few in common with the other networks, suggesting reasons for specificity of cortical dysfunction in FTDP17. This Resource opens up many areas for investigation. All data are available and searchable at http://www.mouseac.org.

show abstract

“…CCI injury versus craniotomy alone in mice also showed signiicant increases in IFN-γ expression with diferent cytokine expression time courses, supporting the impact of injury severity on cytokine expression; the mild injury via craniotomy resulted in a shorter lived cytokine response, while the severe CCI injury resulted in a response persisting for at least 21 days. IFN-γ expression peaked at 3 and 7 days post-injury in CCI-injured and craniotomy mice, respectively, with CCIinjured mice expressing higher peak levels of IFN-γ [150].…”

Section: Inlammatory Interferon-γ In Tbimentioning

confidence: 99%

“…In a 21-day analysis of cytokine expression post-CCI in mice, IL-10 was modestly elevated by day one post-injury with peak expression at 3 days post-CCI [150]. A weight drop model of TBI in rats showed an acute rise of IL-10 brain levels beginning 2 h post-injury followed by a progressive rise beginning at 4 h post-TBI; mRNA expression of IL-10 peaked within minutes post-injury followed by an acute drop and rebound that progressively declined over the remaining 24 h [98].…”

Section: Anti-inlammatory Il-10 In Tbimentioning

confidence: 99%

Roles of Pro- and Anti-inflammatory Cytokines in Traumatic Brain Injury and Acute Ischemic Stroke

Dugue¹,

Nath²,

Dugue³

et al. 2017

Mechanisms of Neuroinflammation

View full text Add to dashboard Cite

This chapter will introduce the reader to the pathophysiology of two devastating neurologic events, traumatic brain injury (TBI) and acute ischemic stroke (AIS). Here we focus on the role of key pro-inlammatory and anti-inlammatory cytokines. Several experimental interventions have been found to modulate cytokine production and brain injury after AIS or TBI. Here minocycline, biological response modiiers, hormonal therapies, omega-3 faty acids, N-acetylcysteine, and cannabinoids will be discussed. In addition, the role of cytokine-induced inlammasomes in both TBI and AIS will be addressed and followed by discussion of pro-inlammatory cytokines (e.g., TNF-α, IL-1β, IL-18, and IFN-γ). Finally, the main anti-inlammatory cytokines, IL-33, IL-10, IL-6, and IL-4, will be discussed in the context of both TBI and AIS. It should be noted that the role of these cytokines is diverse and the dichotomization of classically pro-versus anti-inlammatory cytokines is being re-examined, as many of these cytokines have been found to play dual roles in TBI and AIS brain injury.Keywords: traumatic brain injury, ischemic stroke, cytokines, interleukins, inlammasome Pathophysiology of traumatic brain injuryTraumatic brain injury (TBI) is a major cause of death and disability worldwide [1,2]. It is one of the most commonly diagnosed neurological disorders in the United States, impacting people of a variety of ages and segments of society [3]. In Europe, the economic cost of © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.TBI is over 33 billion euros per year [4]. Continued surveillance and research is being done to reduce primary and secondary TBI [as well as acute ischemic stroke(AIS)]-induced brain injury [1].The pathophysiology of TBI begins with the initial brain trauma (i.e., the primary injury). This primary injury results from mechanical damage that disrupts the blood-brain barrier (BBB), alters the vasculature and damages brain tissue. The resulting injured glia and neurons release their intracellular contents (i.e., damage-associated molecular paterns; (DAMPs)) into the extracellular space and activate neighboring glia and neurons. Activated glia and neurons then produce molecular signals that can both exacerbate and mend the acute injury and contribute to long-term recovery [5][6][7][8][9]. These downstream molecular and cellular processes (i.e., the secondary injury in TBI) are the focus of many pre-clinical and clinical therapeutic studies. Secondary injury in TBI involves a host of molecular and cellular responses to the The pathophysiology of AIS and TBI share common mechanisms. The initial insult in AIS, an occlusion of blood low resulting in a core infarct zone surrounded by a poorly perfused penumbra, versus the initial primary physical impact in TBI both result in pe...

show abstract

Controlled Cortical Impact and Craniotomy Induce Strikingly Similar Profiles of Inflammatory Gene Expression, but with Distinct Kinetics

Cited by 87 publications

References 33 publications

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

A Genome-wide Gene-Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

Roles of Pro- and Anti-inflammatory Cytokines in Traumatic Brain Injury and Acute Ischemic Stroke

Contact Info

Product

Resources

About