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Journals
Biomolecules
Special Issues
The Immune Response to Severe Trauma
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The Immune Response to Severe Trauma

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 1975

Special Issue Editors

Dr. Jon Hazeldine

E-Mail Website
Guest Editor
Department of Inflammation and Ageing, University of Birmingham Research Labs, Queen Elizabeth Hospital, Birmingham, UK
Interests: critical care; traumatic injury; burns; innate immunity; neutrophils; mitochondrial-derived damage-associated molecular patterns; immune dysfunction
Special Issues, Collections and Topics in MDPI journals
Dr. David N Naumann

E-Mail Website
Guest Editor
1. Academic Department of Military Surgery and Trauma, Royal Centre for Defence Medicine, Birmingham, UK
2. Department of Inflammation and Ageing, University of Birmingham, Birmingham, West Midlands, UK
Interests: traumatic injury; endotheliopathy; hemorrhagic shock; coagulopathy; microcirculation; blood transfusion

Special Issue Information

Dear Colleagues,

Severe trauma remains one of the leading causes of death and disability worldwide, with outcomes often dictated not only by the primary injury but also by the host’s immune response. Trauma initiates rapid and profound pro- and anti-inflammatory immunological responses that can protect against infection and aid repair but also predispose patients, in the short and long term, to systemic inflammation, immune suppression, sepsis, and multi-organ failure. Despite progress in resuscitation and critical care, trauma-induced immune dysregulation continues to drive high morbidity and mortality. This Special Issue, entitled “The Immune Response to Severe Trauma”, will explore the molecular mechanisms underpinning post-trauma immune dysregulation as well as the clinical consequences of these immune responses, from early biomarkers of immune dysfunction to therapeutic strategies aimed at modulating immunity for improving patient outcomes. By integrating basic discoveries with translational and clinical research, this collection seeks to advance our understanding of the immediate and long-term immune response to major trauma with the intention of improving the survival and recovery of severely injured patients.

Dr. Jon Hazeldine
Dr. David N Naumann
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • trauma-induced immune response
  • systemic inflammation
  • immune suppression
  • immune dysregulation
  • critical care

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Published Papers (2 papers)

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Research

25 pages, 6745 KB  
Article
Major Traumatic and Severe Thermal Injuries Lead to Immediate and Persistent Elevations in Circulating Concentrations of Resistin That Are Associated with Poor Clinical Outcomes and Impaired Innate Immune Responses
by Emily Horner, Kirsty C. McGee, Sebastian Tullie, David N. Naumann, Animesh Acharjee, Thomas Lissillour, Ali Asiri, Janice M. S. Ng, Jack Sullivan, Amanda V. Sardeli, Paul Harrison, Antonio Belli, Naiem S. Moiemen, Janet M. Lord and Jon Hazeldine
Biomolecules 2026, 16(3), 443; https://doi.org/10.3390/biom16030443 - 16 Mar 2026
Viewed by 727
Abstract
Major trauma induces innate immune suppression, yet the underlying mechanisms are poorly understood. Resistin is an immunosuppressive molecule that is systemically elevated post-injury. However, its role in trauma-induced immune dysfunction and clinical outcomes is poorly defined. Here, we acquired blood samples from 147 [...] Read more.
Major trauma induces innate immune suppression, yet the underlying mechanisms are poorly understood. Resistin is an immunosuppressive molecule that is systemically elevated post-injury. However, its role in trauma-induced immune dysfunction and clinical outcomes is poorly defined. Here, we acquired blood samples from 147 adult trauma patients (≤1, 4–12, 48–72 h post-injury) and 95 burns patients (days 1, 3, 7, 14, 28 post-burn). We measured plasma resistin concentrations, studied resistin gene expression in peripheral blood mononuclear cells (PBMCs) and neutrophils, and measured resistin production by lipopolysaccharide (LPS)-challenged whole blood leukocytes. To identify potential novel triggers of resistin secretion by immune cells, we examined the effect that stimulation with mitochondrial-derived damage-associated molecular patterns (mtDAMPs) had on resistin production by neutrophils isolated from healthy donors. We also treated neutrophils, from healthy donors, and THP-1 cells with resistin prior to stimulation with Phorbol 12-myristate-13-acetate (PMA) or LPS to study its effects on reactive oxygen species (ROS) and cytokine production, respectively. Injured patients presented with significantly elevated circulating resistin concentrations and increased resistin gene expression in PBMCs and neutrophils. LPS and mtDAMP stimulation promoted resistin secretion by whole blood leukocytes and neutrophils. Plasma resistin concentrations were negatively associated with PMA-induced ROS generation by neutrophils, and LPS-induced cytokine production by monocytes. Resistin-treated THP-1 cells and neutrophils exhibited impaired functional responses upon secondary stimulation with LPS or PMA, respectively. Trauma patients who developed multiple organ dysfunction syndrome (MODS) presented with significantly elevated resistin concentrations, which at 48–72 h post-injury showed good performance as a predictor of post-traumatic MODS (AUROC, 0.796). Hyperresistinemia is an immediate and persistent feature of the inflammatory response to injury that may contribute to the development of innate immune dysfunction. Full article
(This article belongs to the Special Issue The Immune Response to Severe Trauma)
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15 pages, 7227 KB  
Article
Traumatic Brain Injury Induces Senescence in Brain Microvasculature
by Tejal Shreeya, Zsófia R. Hernádi, Zsolt K. Bali, Nóra Bruszt, István Hernádi, Bálint Fazekas, Krisztina Amrein, Endre Czeiter, Csilla Fazakas, Imola Wilhelm, István A. Krizbai and Attila E. Farkas
Biomolecules 2026, 16(3), 359; https://doi.org/10.3390/biom16030359 - 28 Feb 2026
Viewed by 869
Abstract
Background: Traumatic brain injury (TBI) frequently leads to long-term neurological deficits. Recent research also implicates cellular senescence—a state of permanent cell cycle arrest driven by DNA damage—as a key contributor to neuroinflammation and cognitive decline. This study investigates the cell-type specificity of senescence [...] Read more.
Background: Traumatic brain injury (TBI) frequently leads to long-term neurological deficits. Recent research also implicates cellular senescence—a state of permanent cell cycle arrest driven by DNA damage—as a key contributor to neuroinflammation and cognitive decline. This study investigates the cell-type specificity of senescence within glial and vascular cells of the neurovascular unit (NVU) following experimental TBI in a rat model. Methods: Rats underwent various TBI scenarios, including single severe TBI (sTBI), single mild TBI (mTBI), repetitive mild TBI (rmTBI) and repetitive sham-operated control (rSham). Twenty-four hours or four weeks later, brains were harvested and brain sections were co-stained for γH2AX and cell type-specific markers. Immunofluorescence microscopy was used to comprehensively assess senescence in both glial and vascular cells of the NVU, specifically astrocytes, microglia, endothelial cells, and pericytes. Results: We observed acute increased astrocyte senescence in sTBI samples and microglial senescence in mTBI and sTBI samples in the neocortex, while endothelial cell senescence was significantly elevated in the neocortex of the sTBI group after four weeks. Pericytes did not exhibit significant signs of senescence at either time point. Conclusion: These findings demonstrate differential γH2AX labelling of NVU components following TBI, suggesting that vulnerability to TBI-induced senescence can be specific both to the cell type and the time after the injury. This has implications on therapies targeting senescent cells for mitigating the long-term consequences of TBI. Full article
(This article belongs to the Special Issue The Immune Response to Severe Trauma)
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