Involvement of Matrix Metalloproteinases (MMP-2 and MMP-9), Inflammasome NLRP3, and Gamma-Aminobutyric Acid (GABA) Pathway in Cellular Mechanisms of Neuroinflammation in PTSD.

Research into the potential health consequences of trauma indicates that traumatic experiences can disrupt normal biological processes and increase the risk of neuroinflammation and the development of clinical symptoms of post-traumatic stress disorder (PTSD). In this study, we examined the relationship between neuroinflammation and three specific biomarkers-matrix metalloproteinases MMP-2 and MMP-9, the inflammasome NLRP3, and the inhibitory neurotransmitter GABA-in connection with PTSD symptoms assessed using the PTSD Symptom Scale-Interview for DSM-5 (PSSI-5). The symptoms were categorized into the following domains: re-experiencing, avoidance, alterations in cognition and mood, increased arousal and reactivity, distress and functional impairment, symptom onset and duration, and the total symptom score. Our findings confirmed the pro-inflammatory roles of MMP-2, MMP-9, and the inflammasome NLRP3, as well as the anti-inflammatory, calming effect of GABA. We identified strong correlations between biomarkers, particularly between MMP-2 and MMP-9, MMP-2 and NLRP3, and MMP-2 and GABA, highlighting a closely interconnected inflammatory response. Among the PSSI-5 domains, re-experiencing, increased arousal and reactivity, and distress and functional impairment showed the strongest associations with the total symptom score. Recent research focusing on these cellular mechanisms has provided valuable insights into the role of neuroinflammation in PTSD. These findings enhance our understanding of how inflammation contributes to the disorder's development and progression.