ArticleStroke and vascular neurology2022
Pertussis toxin-induced inflammatory response exacerbates intracerebral haemorrhage and ischaemic stroke in mice.
Article in Stroke and vascular neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Gain-of-function PPM1D mutations attenuate ischemic stroke.Cell death and differentiation · 2025Article
- Inflammatory Responses Potentiate GAS M Protein Induced Cardiac Damage in an Experimental Model of Rheumatic Heart Disease.Immunity, inflammation and disease · 2025Article
- Neutrophils in Intracerebral Hemorrhage: Roles, Mechanisms, and Therapeutic Implications.Mediators of inflammation · 2025Review
- Astrocyte-derived Interleukin-31 causes poor prognosis in elderly patients with intracerebral hemorrhage.Brain pathology (Zurich, Switzerland) · 2024Article
- Role of Neutrophils as Therapeutic Targets in Intracerebral Hemorrhage.Therapeutic innovation & regulatory science · 2024Review
- Vascular smooth muscle cell-specific Igf1r deficiency exacerbates the development of hypertension-induced cerebral microhemorrhages and gait defects.GeroScience · 2024Article
- Clinical Potential of Immunotherapies in Subarachnoid Hemorrhage Treatment: Mechanistic Dissection of Innate and Adaptive Immune Responses.Aging and disease · 2023Review
- Group 2 innate lymphoid cells resolve neuroinflammation following cerebral ischaemia.Stroke and vascular neurology · 2023Article
- Selenium supplementation provides potent neuroprotection following cerebral ischemia in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- RNA-binding proteins as a common ground for neurodegeneration and inflammation in amyotrophic lateral sclerosis and multiple sclerosis.Frontiers in molecular neuroscience · 2023Review
- Targeting CCL5 signaling attenuates neuroinflammation after seizure.CNS neuroscience & therapeutics · 2023Article
- The hallmark and crosstalk of immune cells after intracerebral hemorrhage: Immunotherapy perspectives.Frontiers in neuroscience · 2022Review
- Natural Compounds for SIRT1-Mediated Oxidative Stress and Neuroinflammation in Stroke: A Potential Therapeutic Target in the Future.Oxidative medicine and cellular longevity · 2022Review
- Multimodal NIRS-MRI reveals cortical hypoperfusion, hypoxia, and mitochondrial changes in a mouse model of autoimmune inflammatory diseases.Imaging neuroscience (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStroke is a devastating disease, including intracerebral haemorrhage (ICH) and ischaemic stroke. Emerging evidences indicate that systemic inflammatory cascades after stroke contribute to brain damage. However, the direct effects and features of systemic inflammation on brain injury, especially comparing between ischaemic and haemorrhagic stroke, are still obscure.
methodsPertussis toxin (PT) was used to build a pro-inflammatory milieu after ICH and ischaemic stroke in mouse model. The neurodeficits, stroke lesion, immune response and blood-brain barrier (BBB) destruction were assessed.
resultsIn ICH mouse model, PT-induced systemic inflammation exacerbated neurological deficits, and enlarged haemorrhage lesion and perihaematomal oedema. We also found promoted leucocyte infiltration and inflammatory cytokine release into the brain after PT treatment. Moreover, the integrity of the BBB was further disrupted after receiving PT. Furthermore, we demonstrated that PT enhanced brain inflammation and aggravated stroke severity in middle cerebral artery occlusion mouse model.
conclusionsOur results suggest that PT increases inflammatory response that exacerbates brain injury after ICH or ischaemic stroke in mouse model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.