Vlad Hârtie, Maria Comănescu, Emilia Pătrășcanu, Andrei Cucu, Lidia Cureniuc, Otilia Boișteanu, Mihaela Dana Turliuc
ABSTRACT
Neuroinflammation is an inflammatory process that occurs in the central nervous system (CNS), including the brain and spinal cord. It can be triggered by various conditions such as traumatic injuries, infections, neurodegenerative diseases (e.g., Alzheimer’s or Parkinson’s), autoimmune disorders, or metabolic stress. In cases of acute traumatic brain injury, neuroinflammation is caused by the primary injury and can exacerbate the evolving tissue pathology. The cells involved in the primary brain injury initiate a series of pathological reactions that involve a response from the immune system. It is this immune response that initiates neuroinflammation and leads to pathological consequences over time.
The immune response varies depending on the injury mechanism, the location of immune cells in the brain, as well as the affected individual. Understanding the signals that initiate neuroinflammation and the context in which they arise can be crucial for understanding the contributions of immune cells in both pathology and regeneration. This article aims to review a number of factors that could influence the behavior of immune cells following acute traumatic brain injuries and the role of Interleukin-6 in neuroinflammation.
DOI : 10.62610/RJOR.2025.2.17.93