We are analyzing https://link.springer.com/article/10.1007/s00281-023-00993-5.

Title:
The role of circulating cell-free DNA as an inflammatory mediator after stroke | Seminars in Immunopathology
Description:
Stroke is the second leading cause of death worldwide and a leading cause of disability. Clinical and experimental studies highlighted the complex role of the immune system in the pathophysiology of stroke. Ischemic brain injury leads to the release of cell-free DNA, a damage-associated molecular pattern, which binds to pattern recognition receptors on immune cells such as toll-like receptors and cytosolic inflammasome sensors. The downstream signaling cascade then induces a rapid inflammatory response. In this review, we are highlighting the characteristics of cell-free DNA and how these can affect a local as well as a systemic response after stroke. For this purpose, we screened literature on clinical studies investigating cell-free DNA concentration and properties after brain ischemia. We report the current understanding for mechanisms of DNA uptake and sensing in the context of post-stroke inflammation. Moreover, we compare possible treatment options targeting cell-free DNA, DNA-sensing pathways, and the downstream mediators. Finally, we describe clinical implications of this inflammatory pathway for stroke patients, open questions, and potential future research directions.
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Keywords {🔍}

pubmed, stroke, article, google, scholar, dna, cas, cfdna, central, aim, patients, ischemic, blood, tlr, cellfree, dnase, activation, inflammasome, immune, studies, injury, response, clinical, brain, cell, systemic, cells, binding, inflammatory, plasma, concentrations, release, inflammation, increased, outcome, treatment, tissue, hmgb, signaling, ilβ, receptor, circulating, sensing, pathway, leads, concentration, acute, cgas, human, experimental,

Topics {✒️}

post-stroke double-strand cfdna c-type lectin-receptor-2d ischemia-reperfusion injury-induced myocardial preclinical deep-vein thrombosis cgas-sting-mediated interferon response cytokine-induced sickness behavior nf-kb signaling pathway neuroprotective steroids 17β-estradiol article download pdf cerebral ischemia/reperfusion injury cell-free deoxyribonucleic acid cell-free dna comprises dsdna = double-stranded dna k-rich histone tail long-term recovery index nf-κb-mediated transcription cyclic gmp-amp synthase circulating cell-free dna tissue-specific cell death dna-stimulated cell death rupture-prone carotid-plaques neutrophil extracellular traps cells releasing tnf-α recruit tank-binding kinase short-term neurological outcome nf-kappab activation intra-tumoral dendritic cells fetal cell-free dna microglial cgas-sting pathway quantitative real-time pcr sputum cell-free dna mrs = modified rankin score cell-free plasma dna sense dna-bound proteins myd88-dependent signaling cascade 4-sulfonic calixarenes proinflammatory cytokine il-1β tlr9-p38 mapk signaling tissue-type plasminogen activator cell death–derived cfdna short-term disease severity cfdna-driven immunological cascade systemic immune alterations recent post-stroke therapy serum cell-free dna anti-il-1β treatment proinflammatory cytokine il-β il-1β neutralization analyzed post-injury immunosuppression subcutaneous il-1ra application

Schema {🗺️}

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         headline:The role of circulating cell-free DNA as an inflammatory mediator after stroke
         description:Stroke is the second leading cause of death worldwide and a leading cause of disability. Clinical and experimental studies highlighted the complex role of the immune system in the pathophysiology of stroke. Ischemic brain injury leads to the release of cell-free DNA, a damage-associated molecular pattern, which binds to pattern recognition receptors on immune cells such as toll-like receptors and cytosolic inflammasome sensors. The downstream signaling cascade then induces a rapid inflammatory response. In this review, we are highlighting the characteristics of cell-free DNA and how these can affect a local as well as a systemic response after stroke. For this purpose, we screened literature on clinical studies investigating cell-free DNA concentration and properties after brain ischemia. We report the current understanding for mechanisms of DNA uptake and sensing in the context of post-stroke inflammation. Moreover, we compare possible treatment options targeting cell-free DNA, DNA-sensing pathways, and the downstream mediators. Finally, we describe clinical implications of this inflammatory pathway for stroke patients, open questions, and potential future research directions.
         datePublished:2023-05-22T00:00:00Z
         dateModified:2023-05-22T00:00:00Z
         pageStart:411
         pageEnd:425
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            Tissue injury
            Stroke
            Inflammation
            Inflammasome
            Immunology
            Internal Medicine
            Pathology
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ScholarlyArticle:
      headline:The role of circulating cell-free DNA as an inflammatory mediator after stroke
      description:Stroke is the second leading cause of death worldwide and a leading cause of disability. Clinical and experimental studies highlighted the complex role of the immune system in the pathophysiology of stroke. Ischemic brain injury leads to the release of cell-free DNA, a damage-associated molecular pattern, which binds to pattern recognition receptors on immune cells such as toll-like receptors and cytosolic inflammasome sensors. The downstream signaling cascade then induces a rapid inflammatory response. In this review, we are highlighting the characteristics of cell-free DNA and how these can affect a local as well as a systemic response after stroke. For this purpose, we screened literature on clinical studies investigating cell-free DNA concentration and properties after brain ischemia. We report the current understanding for mechanisms of DNA uptake and sensing in the context of post-stroke inflammation. Moreover, we compare possible treatment options targeting cell-free DNA, DNA-sensing pathways, and the downstream mediators. Finally, we describe clinical implications of this inflammatory pathway for stroke patients, open questions, and potential future research directions.
      datePublished:2023-05-22T00:00:00Z
      dateModified:2023-05-22T00:00:00Z
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      pageEnd:425
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         Cell-free DNA
         Tissue injury
         Stroke
         Inflammation
         Inflammasome
         Immunology
         Internal Medicine
         Pathology
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      name:Saskia R. Wernsdorf
      affiliation:
            name:University Hospital, LMU Munich
            address:
               name:Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany
               type:PostalAddress
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      name:Arthur Liesz
      url:http://orcid.org/0000-0002-9069-2594
      affiliation:
            name:University Hospital, LMU Munich
            address:
               name:Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany
               type:PostalAddress
            type:Organization
            name:Munich Cluster for Systems Neurology (SyNergy)
            address:
               name:Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
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      email:[email protected]
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      name:Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany
      name:Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany
      name:Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany
      name:Munich Cluster for Systems Neurology (SyNergy), Munich, Germany

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