THE ROLE OF INFLAMMATORY RESPONSE IN MILD TRAUMATIC BRAIN INJURY – A NARRATIVE REVIEW
IOANNIS MAVROUDIS 1,2,3, WALTHER BILD 5,7*, FOIVOS PETRIDIS 2, SIMELA CHATZIKONSTANTINOU 2, DIMITRIOS KAZIS 2, GABRIEL DĂSCĂLESCU 4,6, ALIN CIOBICA 3,4,6,7, ANTONETA DACIA PETROAIE 5, DRAGOS LUCIAN GORGAN 6, DANIELA CARMEN ABABEI 5, RAZVAN-NICOLAE RUSU 5, VERONICA BILD 5,7
1 Department of Neuroscience, Leeds Teaching Hospitals, NHS Trust, Leeds LS9 7TF, UK
2 Third Department of Neurology, Aristotle University of Thessaloniki, Greece
3 Academy of Romanian Scientists, Splaiul Independentei nr. 54, Sector 5, Bucuresti, Romania
4 Preclinical Department, Apollonia University, Păcurari Street 11, Iași, Romania
5 “Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania
6 Department of Biology, Faculty of Biology, Alexandru Ioan Cuza University of Iasi, B dul Carol I, No. 11, Iasi, Romania
7 “Olga Necrasov” Centre of Anthropological and Biomedical Research, Romanian Academy, B-dul Carol I, No. 8, Iasi, Romania
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Mild traumatic brain injury (mTBI) represents one of the most prevalent neurological conditions worldwide, yet its long-term consequences remain incompletely understood. Growing evidence suggests that inflammation plays a crucial role in both the acute and chronic phases of mTBI, linking neuroimmune processes to symptom persistence and the risk of secondary pathologies. This narrative review aims to provide an updated synthesis of the molecular and cellular mechanisms underlying the inflammatory response in mTBI, with a particular focus on neuroinflammation, systemic cytokine dynamics and their association with injury severity and chronic outcomes. A comprehensive literature search was conducted across major biomedical databases, including PubMed, Scopus and Web of Science, to identify relevant experimental and clinical studies published in the last two decades. Emphasis was placed on reports addressing systemic and central inflammatory markers, microglial activation and therapeutic strategies targeting inflammation in mTBI. Evidence demonstrates that systemic cytokines are significantly elevated following mTBI, with some persisting up to one year post-injury. Microglia emerge as a central modulator of neuroinflammation due to their plasticity and multifactorial repertoire, while astrocytes, peripheral immune cells and endothelial components also contribute to the inflammatory cascade. The interplay between systematic and central responses appears to influence both symptom duration and long-term neurological risk. Understanding the inflammatory response in mTBI highlights the urgent need for novel and selective anti-inflammatory therapies. Targeted interventions hold promise not only for improving acute recovery but also for preventing chronic neuropsychiatric and neurodegenerative sequelae in patients with mTBI.
