Early monitoring and quantitative evaluation of macrophage infiltration after experimental traumatic brain injury: A magnetic resonance imaging and flow cytometric analysis

Mishra, Sushanta Kumar; Kumar, B.S. Hemanth; Khushu, Subash; Singh, Ajay K.; Gangenahalli, Gurudutta

doi:10.1016/j.mcn.2016.11.008

Cited by 34 publications

(23 citation statements)

References 40 publications

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“…Values are mean ± SD; n = 4 to 6, **P < .01 vs WT sham onset. 16,17 The present study revealed that most unilateral T2-hyperintensity lesions were on the right side, the opposite side to the endovascular perforation. In addition, we have the data that T2 hyperintensity in white matter is found bilaterally at 24 hours after SAH.…”

Section: Discussionsupporting

confidence: 50%

“…In experimental cerebral ischemia, T2‐hyperintensity lesions appear 24 hours after transient middle cerebral artery occlusion . In contrast, in experimental traumatic brain injury, T2‐hyperintensity lesions are already recognized at 6 hours after onset . The present study revealed that most unilateral T2‐hyperintensity lesions were on the right side, the opposite side to the endovascular perforation.…”

Section: Discussionmentioning

confidence: 42%

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White matter T2 hyperintensities and blood‐brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin‐2

Toyota

Wei

et al. 2019

CNS Neurosci Ther

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Aims The current study examined whether white matter injury occurs in the hyperacute (4 hours) phase after subarachnoid hemorrhage (SAH) and the potential role of blood‐brain barrier (BBB) disruption and an acute phase protein, lipocalin 2 (LCN2), in that injury. Methods Subarachnoid hemorrhage was induced by endovascular perforation in adult mice. First, wild‐type (WT) mice underwent MRI 4 hours after SAH to detect white matter T2 hyperintensities. Second, changes in LCN2 expression and BBB disruption associated with the MRI findings were examined. Third, SAH‐induced white matter injury at 4 hours was compared in WT and LCN2 knockout (LCN2 KO) mice. Results At 4 hours, most animals had uni‐ or bilateral white matter T2 hyperintensities after SAH in WT mice that were associated with BBB disruption and LCN2 upregulation. However, some disruption and LCN2 upregulation was also found in mice with no T2‐hyperintensity lesion. In contrast, there were no white matter T2 hyperintensities in LCN2 KO mice after SAH. LCN2 deficiency also attenuated BBB disruption, myelin damage, and oligodendrocyte loss. Conclusions Subarachnoid hemorrhage causes very early BBB disruption and LCN2 expression in white matter that is associated with and may precede T2 hyperintensities. LCN2 deletion attenuates MRI changes and pathological changes in white matter after SAH.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 42%

White matter T2 hyperintensities and blood‐brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin‐2

Toyota

Wei

et al. 2019

CNS Neurosci Ther

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“…CNS injury also induces macrophage recruitment from the periphery, whose role is to rapidly access the injury site as a first line of defense against infection (Corps et al 2015; Mishra et al 2016). Comprehensively differentiating these two cell populations is difficult, but they do differ in their morphological and phenotypical classification.…”

Section: Introductionmentioning

confidence: 99%

Sexual dimorphism in the inflammatory response to traumatic brain injury

Villapol

Loane

Burns

2017

Glia

241

223

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The activation of resident microglial cells, alongside the infiltration of peripheral macrophages, are key neuroinflammatory responses to traumatic brain injury (TBI) that are directly associated with neuronal death. Sexual disparities in response to TBI have been previously reported, however it is unclear whether a sex difference exists in neuroinflammatory progression after TBI. We exposed male and female mice to moderate-to-severe controlled cortical impact injury and studied glial cell activation in the acute and chronic stages of TBI using immunofluorescence and in situ hybridization analysis. We found that the sex response was completely divergent up to 7 days post-injury. TBI caused a rapid and pronounced cortical microglia/macrophage activation in male mice with a prominent activated phenotype that produced both pro- (IL-1β and TNFα) and anti-inflammatory (Arg1 and TGFβ) cytokines with a single-phase, sustained peak from 1 to 7 days. In contrast, TBI caused a less robust microglia/macrophage phenotype in females with biphasic pro-inflammatory response peaks at 4 hours and 7 days, and a delayed anti-inflammatory mRNA peak at 30 days. We further report that female mice were protected against acute cell loss after TBI, with male mice demonstrating enhanced astrogliosis, neuronal death, and increased lesion volume through 7 days post-TBI. Collectively, these findings indicate that TBI leads to a more aggressive neuroinflammatory profile in male compared to female mice during the acute and sub-acute phases post-injury. Understanding how sex affects the course of neuroinflammation following brain injury is a vital step toward developing personalized and effective treatments for TBI.

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“…Immediately following the mechanical stress (primary injury), several cellular and biochemical pathological events (secondary injury), including oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis occur within minutes and may last from hours to days or months [ 2 ]. Among these pathological changes, neuroinflammation has been implicated as an important secondary injury mechanism that exerts either detrimental or beneficial roles in the process of TBI-induced central nervous system (CNS) damage [ 3 ]. CNS inflammation is a robust, sterile immune reaction that is characterized by CNS-resident glial activation, peripheral immune cells recruitment, and production of cytokines and chemokines [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory and immunomodulatory mechanisms of atorvastatin in a murine model of traumatic brain injury

Gao

Cheng

et al. 2017

J Neuroinflammation

171

111

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Background: Neuroinflammation is an important secondary injury mechanism that has dual beneficial and detrimental roles in the pathophysiology of traumatic brain injury (TBI). Compelling data indicate that statins, a group of lipid-lowering drugs, also have extensive immunomodulatory and anti-inflammatory properties. Among statins, atorvastatin has been demonstrated as a neuroprotective agent in experimental TBI; however, there is a lack of evidence regarding its effects on neuroinflammation during the acute phase of TBI. The current study aimed to evaluate the effects of atorvastatin therapy on modulating the immune reaction, and to explore the possible involvement of peripheral leukocyte invasion and microglia/macrophage polarization in the acute period post-TBI.

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Early monitoring and quantitative evaluation of macrophage infiltration after experimental traumatic brain injury: A magnetic resonance imaging and flow cytometric analysis

Cited by 34 publications

References 40 publications

White matter T2 hyperintensities and blood‐brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin‐2

White matter T2 hyperintensities and blood‐brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin‐2

Sexual dimorphism in the inflammatory response to traumatic brain injury

Anti-inflammatory and immunomodulatory mechanisms of atorvastatin in a murine model of traumatic brain injury

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