Neuroinflammation: The Devil Is in the Details

DiSabato, Damon J.; Quan, Ning; Godbout, Jonathan P.

doi:10.1111/jnc.13607

Cited by 1,640Neuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury and Neurovascular DisturbancesTryptophan and brain disorders

Neuroinflammation: The Devil Is in the Details

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DiSabato, Damon J., Quan, Ning, Godbout, Jonathan P.·2016·Journal of Neurochemistry

DOI 10.1111/jnc.13607PMC PMC5025335

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Abstract

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

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The resting microglia determines the nature of the innate immune response in retinal spaces and is the key checkpoint between limiting or aggravating neuroinflammation.
“The “immune sentinel” of the retina, the resting microglia, determines the nature of the innate immune response in these spaces and is the key checkpoint between limiting or aggravating neuroinflammation [66].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [66]
Inflammatory immune responses for ocular gene therapies become harder to predict in the clinical setting, as both physiological and barrier functions of immune privilege may already be compromised by aging or the ocular disorder physiopathological conditions such as inflammation or oxidative stress induction.
“Inflammatory immune responses for ocular gene therapies become harder to predict in the clinical setting, as both physiological and barrier functions of immune privilege may already be compromised by aging or the ocular disorder physiopathological conditions such as inflammation or oxidative stress induction [21,66,67].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [66]

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“Furthermore, persistent changes in microglia and astrocytes after penetrating TBI, such as increased MHC II expression in rats 16 days post-injury, are caused by CCI (Holmin et al. 1995).”
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The Bacterial Endotoxin Lipopolysaccharide has the Ability to Target the Brain in Upregulating Its Membrane CD14 Receptor Within Specific Cellular Populations
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Cell Death after Spinal Cord Injury Is Exacerbated by Rapid TNFα-Induced Trafficking of GluR2-Lacking AMPARs to the Plasma Membrane
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Acute Minocycline Treatment Mitigates the Symptoms of Mild Blast-Induced Traumatic Brain Injury
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Downregulation of IL-4-induced signalling in hippocampus contributes to deficits in LTP in the aged rat
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Cognitive deficits develop 1 month after diffuse brain injury and are exaggerated by microglia-associated reactivity to peripheral immune challenge
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Microglial activation in healthy aging
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Neuroinflammation and Peripheral Immune Infiltration in Parkinson's Disease: An Autoimmune Hypothesis
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Perisomatic Thalamic Axotomy After Diffuse Traumatic Brain Injury Is Associated With Atrophy Rather Than Cell Death
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Godbout JP Moreau M Lestage J Aging exacerbates depressive-like behavior in mice in response to activation of the peripheral innate immune system. Neuropsychopharmacology 2008b 33 2341 2351 18075491 PMC2907915
Tynan RJ Naicker S Hinwood M Nalivaiko E Buller KM Pow DV Day TA Walker FR Chronic stress alters the density and morphology of microglia in a subset of stress-responsive brain regions. Brain Behav Immun 2010b 24 1058 1068 20153418
Wohleb ES Hanke ML Corona AW Powell ND Stiner LM Bailey MT Nelson RJ Godbout JP Sheridan JF β-Adrenergic receptor antagonism prevents anxiety-like behavior and microglial reactivity induced by repeated social defeat. J Neurosci 2011b 31 6277 6288 21525267 PMC3160240

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Background
Butyrate and Dietary Soluble Fiber Improve Neuroinflammation Associated With Aging in Mice
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Background
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Authors: DiSabato, D. J., Quan, N., & Godbout, J. P.
Affiliations: The Ohio State University (US)
Corresponding author: Godbout, Jonathan P.
ORCID: DiSabato, Damon J.
Quan, Ning
Godbout, Jonathan P.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2016-05-04
Volume: 139
Issue: S2
Pages: 136-153
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1111/jnc.13607
PMC: PMC5025335
OpenAlex: W2302151110
Cited by: 1,640
References: 202
Citations by year: 2026: 159 · 2025: 241 · 2024: 297 · 2023: 265 · 2022: 235 · 2021: 194 · 2020: 129 · 2019: 65 · 2018: 25 · 2017: 22 · 2016: 6 · 2013: 1
FWCI: 3.45
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (R01‐AG‐033028)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords: neuroinflammation, microglia, spinal cord injury, brain injury, stress, aging, functional recovery, central nervous system injury
MeSH terms: Aging, Animals, Brain, Humans, Inflammation, Spinal Cord, Microglia, Neurodegenerative Diseases

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Neuroinflammation: The Devil Is in the Details

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