Neutrophil Dynamics in Trauma-Induced Inflammation
Summary
Traumatic injury triggers an immediate and complex innate immune response in which neutrophils are central mediators. Upon vascular damage and release of damage-associated molecular patterns (DAMPs), neutrophils are rapidly mobilised from the bone marrow and marginated pools, migrating through the endothelium into injured tissues. There they execute antimicrobial and debris-clearing functions through phagocytosis, degranulation and reactive oxygen species generation. Concurrently, neutrophil extracellular trap formation and release of proteolytic enzymes help contain damage but may also contribute to secondary tissue injury and vascular leakage. Throughout this process, neutrophils display marked phenotypic plasticity and heterogeneity, adopting distinct activation states that balance pro-inflammatory clearance with resolution and tissue repair. Dysregulation of this balance underlies systemic inflammatory response syndrome, immune paralysis and organ dysfunction after severe trauma. Advances in flow cytometry, molecular profiling and biomarker discovery are now illuminating the kinetics of neutrophil subsets, their surface receptors and epigenetic modifications, offering new routes to prognostic assays and tailored immunomodulatory interventions.
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Neutrophil Dynamics in Trauma-Induced Inflammation publication trend
The graph below shows the total number of articles in neutrophil dynamics in trauma-induced inflammation across all publications each year (not limited to Nature Index journals).
Technical terms
Neutrophil elastase (NE): A serine protease released from neutrophil granules that degrades extracellular matrix and microbial proteins.
Myeloperoxidase (MPO): A haem-containing enzyme in neutrophil azurophilic granules that generates reactive oxidants for microbial killing.
Citrullinated histone H3 (CitH3): A marker of neutrophil extracellular trap formation, reflecting chromatin decondensation and citrullination of histone H3.
Adhesion G protein–coupled receptor EMR2: A surface receptor upregulated on neutrophils post-trauma, involved in cell adhesion and activation signalling.
Damage-associated molecular pattern (DAMP): Endogenous molecules released by injured cells that trigger innate immune activation through pattern-recognition receptors.
References
- Update on Neutrophil Function in Severe Inflammation. Frontiers in Immunology (2018).
- Elevation of neutrophil‐derived factors in patients after multiple trauma. Journal of Cellular and Molecular Medicine (2023).
- The Posttraumatic Increase of the Adhesion GPCR EMR2/ADGRE2 on Circulating Neutrophils Is Not Related to Injury Severity. Cells (2023).
- Histone H3 posttranslational modified enzymes defined neutrophil plasticity and their vulnerability to IL-10 in the course of the inflammation. Journal of Inflammation (2024).
- Neutrophil heterogeneity and its role in infectious complications after severe trauma. World Journal of Emergency Surgery (2019).
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