Pattern recognition receptors and central nervous system repair

Kigerl, Kristina A.; Vaccari, Juan Pablo de Rivero; Dietrich, W. Dalton; Popovich, Phillip G.; Keane, Robert W.

doi:10.1016/j.expneurol.2014.01.001

Cited by 398 publications

(315 citation statements)

References 142 publications

(196 reference statements)

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“…The translational relevance of these findings is bolstered by knowledge that in IBS, there is evidence of lowgrade immune activation that is associated with gut microbiota alterations ) and increased kynurenine pathway metabolism (Clarke et al, 2009a;Clarke et al, 2012b;Fitzgerald et al, 2008). Interestingly, TLRs are also expressed in the CNS (Kigerl et al, 2014) where they play a role, for example, in visceral pain following chronic stress (Tramullas et al, 2014) and the TLR3 ligand poly(I:C) induces the expression of IDO in human astrocytes (Suh et al, 2007).…”

Section: The Immune System the Gut Microbiota And Implications For Kmentioning

confidence: 99%

Kynurenine pathway metabolism and the microbiota-gut-brain axis

et al. 2017

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Section: The Immune System the Gut Microbiota And Implications For Kmentioning

confidence: 99%

Kynurenine pathway metabolism and the microbiota-gut-brain axis

et al. 2017

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“…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.…”

Section: Pathophysiology Of Traumatic Brain Injurymentioning

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

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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...

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“…Once activated, glial cells have the capacity to induce numerous other receptors and inflammatory mediators following stimulation from other CNS cells, infiltrating leukocytes, and/or invading pathogens [1] . Additionally, both microglia and astrocytes display an array of receptors involved in innate immunity and damage detection, including Toll-like receptors (TLRs), nucleotide-binding oligomerization domains, double-stranded RNA-dependent protein kinases, scavenger receptors, and mannose receptors [122,123] , and summarized in Table 2.…”

Section: Immune Function Of Astrocytesmentioning

confidence: 99%

New advances on glial activation in health and disease

Lee

MacLean

2015

WJV

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In addition to being the support cells of the central nervous system (CNS), astrocytes are now recognized as active players in the regulation of synaptic function, neural repair, and CNS immunity. Astrocytes are among the most structurally complex cells in the brain, and activation of these cells has been shown in a wide spectrum of CNS injuries and diseases. Over the past decade, research has begun to elucidate the role of astrocyte activation and changes in astrocyte morphology in the progression of neural pathologies, which has led to glial-specific interventions for drug development. Future therapies for CNS infection, injury, and neurodegenerative disease are now aimed at targeting astrocyte responses to such insults including astrocyte activation, astrogliosis and other morphological changes, and innate and adaptive immune responses.

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Pattern recognition receptors and central nervous system repair

Cited by 398 publications

References 142 publications

Kynurenine pathway metabolism and the microbiota-gut-brain axis

Kynurenine pathway metabolism and the microbiota-gut-brain axis

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

New advances on glial activation in health and disease

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