ArticleFrontiers in immunology2015
Cardiac Arrest Disrupts Caspase-1 and Patterns of Inflammatory Mediators Differently in Skin and Muscle Following Localized Tissue Injury in Rats: Insights from Data-Driven Modeling.
Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Age-related exacerbation of lung damage after trauma is associated with increased expression of inflammasome components.Frontiers in immunology · 2023Article
- Broader Insights into Understanding Tumor Necrosis Factor and Neurodegenerative Disease Pathogenesis Infer New Therapeutic Approaches.Journal of Alzheimer's disease : JAD · 2021Review
- Inflammasomes in Tissue Damages and Immune Disorders After Trauma.Frontiers in immunology · 2018Review
- Inflammation Following Traumatic Brain Injury in Humans: Insights from Data-Driven and Mechanistic Models into Survival and Death.Frontiers in pharmacology · 2016Article
- Reverse Engineering the Inflammatory "Clock": From Computational Modeling to Rational Resetting.Drug discovery today. Disease models · 2016Article
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundTrauma often cooccurs with cardiac arrest and hemorrhagic shock. Skin and muscle injuries often lead to significant inflammation in the affected tissue. The primary mechanism by which inflammation is initiated, sustained, and terminated is cytokine-mediated immune signaling, but this signaling can be altered by cardiac arrest. The complexity and context sensitivity of immune signaling in general has stymied a clear understanding of these signaling dynamics. METHODOLOGY/PRINCIPAL
findingsWe hypothesized that advanced numerical and biological function analysis methods would help elucidate the inflammatory response to skin and muscle wounds in rats, both with and without concomitant shock. Based on the multiplexed analysis of inflammatory mediators, we discerned a differential interleukin (IL)-1α and IL-18 signature in skin vs. muscle, which was suggestive of inflammasome activation in the skin. Immunoblotting revealed caspase-1 activation in skin but not muscle. Notably, IL-1α and IL-18, along with caspase-1, were greatly elevated in the skin following cardiac arrest, consistent with differential inflammasome activation. CONCLUSION/SIGNIFICANCE: Tissue-specific activation of caspase-1 and the NLRP3 inflammasome appear to be key factors in determining the type and severity of the inflammatory response to tissue injury, especially in the presence of severe shock, as suggested via data-driven modeling.
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