Alcohol exposure–induced neurovascular inflammatory priming impacts ischemic stroke and is linked with brain perivascular macrophages

Drieu, Antoine; Lanquetin, Anastasia; Levard, Damien; Glavan, Martina; Campos, Francisco; Quenault, Aurélien; Lemarchand, Eloïse; Naveau, Mikaël; Pitel, Anne‐Lise; Castillo, José; Vivien, Denis; Rubio, Marina

doi:10.1172/jci.insight.129226

Cited by 23 publications

(22 citation statements)

References 48 publications

(58 reference statements)

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“…Neutrophils are the first bloodborne immune cells to invade the ischemic tissue, followed by monocytes. The sequence of leukocyte recruitment into the brain after experimental stroke has been well characterized ( Gelderblom et al, 2009 , Drieu et al, 2020a , Drieu et al, 2020b ), whereas the temporal and spatial profile of the immune cell recruitment after stroke in humans requires better characterization ( Veltkamp and Gill, 2016 ).…”

Section: Main Actors On Stroke Inflammatory and Immune Responsesmentioning

confidence: 99%

“…Moreover, neutrophil extracellular traps (NETs; networks of DNA, histones and proteolytic enzymes) secreted by neutrophils are capable of activating platelets and contribute to the thrombotic processes ( Rayasam et al, 2018 ). Clinical data and experimental models of stroke have shown that neutrophils infiltrate the brain parenchyma within hours of stroke onset ( Gelderblom et al, 2009 , Drieu et al, 2020a , Drieu et al, 2020b , Cai et al, 2020 ). Furthermore, clinical studies demonstrated that the neutrophil-to-lymphocyte ratio might be a strong prognostic marker in acute ischemic stroke ( Xue et al, 2017 ) and that the NETs are increased in patients with stroke ( Vallés et al, 2017 ).…”

Section: Main Actors On Stroke Inflammatory and Immune Responsesmentioning

confidence: 99%

“…Infiltrating γδ T, CD8 + T, and NK cells contribute to the acute brain injury after stroke onset, while regulatory T and B cells are reported to be protective ( Feng et al, 2017 ). Experimental models of stroke have shown that lymphocyte infiltration into the ischemic tissue comes later after stroke onset, starting at day 3 ( Drieu et al, 2020a , Drieu et al, 2020b ). Postmortem human samples have shown that lymphocyte infiltration into the ischemic area occurs from day 3 and can be present up to 53 years after stroke ( Mena et al, 2004 ).…”

Section: Main Actors On Stroke Inflammatory and Immune Responsesmentioning

confidence: 99%

“…Another model of thromboembolic stroke consists in injecting thrombin directly into the MCA by using a micropipette, which causes the in situ formation of a fibrin-rich clot ( Orset et al, 2007 , Le Behot et al, 2014 ). These fibrin-rich clots may be spontaneously lysed (partially or completely), as occurs in non-treated patients ( Drieu et al, 2020a , Drieu et al, 2020b ). Infarct volume and localization after both ferric chloride and thrombin models correspond to ischemic brain lesions in the majority of human strokes in proportion to brain size.…”

Section: Experimental Basis For the Clinical Trials On Immunomodulatomentioning

confidence: 99%

“…These cellular responses are accompanied by EC activation at 24 h-48 h that is not present later on (5 days after stroke onset). Whereas ischemic lesions are maximal at 24–48 h after stroke onset, BBB leakage progressively increases with time, being maximal at 5 days after stroke ( Drieu et al, 2020a , Drieu et al, 2020b ).…”

Section: Experimental Basis For the Clinical Trials On Immunomodulatomentioning

confidence: 99%

See 4 more Smart Citations

Filling the gaps on stroke research: Focus on inflammation and immunity

Levard

Buendía

Lanquetin

et al. 2021

Brain, Behavior, and Immunity

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Highlights The different experimental approaches may model different aspects of stroke. Drugs need to be tested in several clinically relevant experimental stroke models. Clot composition, type of arterial occlusion and recanalization need to be considered. Outcomes should include acute but also long-term measurements. Both infarct volume and behavioral deficits need to be systematically measured. Including coexisting risk factors in preclinical stroke research is mandatory. Performing multicenter studies may increase the reliability of preclinical results.

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Section: Main Actors On Stroke Inflammatory and Immune Responsesmentioning

confidence: 99%

Section: Main Actors On Stroke Inflammatory and Immune Responsesmentioning

confidence: 99%

Section: Main Actors On Stroke Inflammatory and Immune Responsesmentioning

confidence: 99%

Section: Experimental Basis For the Clinical Trials On Immunomodulatomentioning

confidence: 99%

Section: Experimental Basis For the Clinical Trials On Immunomodulatomentioning

confidence: 99%

See 3 more Smart Citations

Filling the gaps on stroke research: Focus on inflammation and immunity

Levard

Buendía

Lanquetin

et al. 2021

Brain, Behavior, and Immunity

Self Cite

View full text Add to dashboard Cite

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Role of microglia in stroke

Planas

2024

Glia

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Microglia play key roles in the post‐ischemic inflammatory response and damaged tissue removal reacting rapidly to the disturbances caused by ischemia and working to restore the lost homeostasis. However, the modified environment, encompassing ionic imbalances, disruption of crucial neuron–microglia interactions, spreading depolarization, and generation of danger signals from necrotic neurons, induce morphological and phenotypic shifts in microglia. This leads them to adopt a proinflammatory profile and heighten their phagocytic activity. From day three post‐ischemia, macrophages infiltrate the necrotic core while microglia amass at the periphery. Further, inflammation prompts a metabolic shift favoring glycolysis, the pentose‐phosphate shunt, and lipid synthesis. These shifts, combined with phagocytic lipid intake, drive lipid droplet biogenesis, fuel anabolism, and enable microglia proliferation. Proliferating microglia release trophic factors contributing to protection and repair. However, some microglia accumulate lipids persistently and transform into dysfunctional and potentially harmful foam cells. Studies also showed microglia that either display impaired apoptotic cell clearance, or eliminate synapses, viable neurons, or endothelial cells. Yet, it will be essential to elucidate the viability of engulfed cells, the features of the local environment, the extent of tissue damage, and the temporal sequence. Ischemia provides a rich variety of region‐ and injury‐dependent stimuli for microglia, evolving with time and generating distinct microglia phenotypes including those exhibiting proinflammatory or dysfunctional traits and others showing pro‐repair features. Accurate profiling of microglia phenotypes, alongside with a more precise understanding of the associated post‐ischemic tissue conditions, is a necessary step to serve as the potential foundation for focused interventions in human stroke.

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Immune compartments at the brain’s borders in health and neurovascular diseases

et al. 2023

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Recent evidence implicates cranial border immune compartments in the meninges, choroid plexus, circumventricular organs, and skull bone marrow in several neuroinflammatory and neoplastic diseases. Their pathogenic importance has also been described for cardiovascular diseases such as hypertension and stroke. In this review, we will examine the cellular composition of these cranial border immune niches, the potential pathways through which they might interact, and the evidence linking them to cardiovascular disease.

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Alcohol exposure–induced neurovascular inflammatory priming impacts ischemic stroke and is linked with brain perivascular macrophages

Cited by 23 publications

References 48 publications

Filling the gaps on stroke research: Focus on inflammation and immunity

Filling the gaps on stroke research: Focus on inflammation and immunity

Role of microglia in stroke

Immune compartments at the brain’s borders in health and neurovascular diseases

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