Anti-Inflammatory Mechanisms in Critical Care Systems
Summary
The management of life-threatening conditions such as sepsis, acute respiratory distress syndrome and multi-organ trauma relies on the timely restoration of immune homeostasis to prevent overwhelming inflammation and tissue injury. Anti-inflammatory mechanisms in critical care encompass endogenous pathways including the release of specialised pro-resolving mediators, activation of redox-sensitive transcription factors and up-regulation of regulatory immune cells. At a molecular level, nuclear factor kappa B (NF-κB) inhibition and induction of the nuclear factor erythroid 2-related factor 2 (NRF2) programme attenuate cytokine storms, while blockade of the NLR family pyrin domain containing 3 (NLRP3) inflammasome reduces interleukin-1β maturation. Cellular mediators such as regulatory T cells, M2 macrophages and tolerogenic dendritic cells secrete anti-inflammatory cytokines (interleukin-10, transforming growth factor-β) and limit leukocyte recruitment. Therapeutic strategies under investigation include small molecules that chelate danger-associated molecular patterns like high mobility group box 1 (HMGB1), biologics that neutralise pro-inflammatory cytokines, and cell-based therapies using mesenchymal stromal cell exosomes. Collectively, these interventions aim to restore vascular integrity, preserve mitochondrial function and prevent organ dysfunction in critically ill patients.
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Anti-Inflammatory Mechanisms in Critical Care Systems publication trend
The graph below shows the total number of articles in anti-inflammatory mechanisms in critical care systems across all publications each year (not limited to Nature Index journals).
Technical terms
NLRP3 inflammasome: A cytosolic multiprotein complex that activates caspase-1 to process pro-interleukin-1β and pro-interleukin-18 into their mature forms, driving inflammation.
HMGB1: A nuclear alarmin released by damaged or activated cells that acts as a danger-associated molecular pattern to amplify inflammatory responses.
NF-κB: A transcription factor family central to the induction of pro-inflammatory gene expression, including cytokines and adhesion molecules.
NRF2: A redox-sensitive transcription factor that induces antioxidant and cytoprotective genes to counteract oxidative stress and inflammation.
References
- NRF2 Plays a Crucial Role in the Tolerogenic Effect of Ethyl Pyruvate on Dendritic Cells. International Journal of Molecular Sciences (2024).
- Ethyl Pyruvate Inhibits HMGB1 Phosphorylation and Release by Chelating Calcium. Molecular Medicine (2014).
- Ethyl pyruvate protects against sepsis-associated encephalopathy through inhibiting the NLRP3 inflammasome. Molecular Medicine (2020).
- Identification of ethyl pyruvate as a NLRP3 inflammasome inhibitor that preserves mitochondrial integrity. Molecular Medicine (2018).
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