Systemic inflammation and its associations in acute moderate-severe Traumatic Brain Injury: a cross-sectional study

Area of Science:

• Neuroscience
• Immunology
• Biomarkers

Background:

• Traumatic Brain Injury (TBI) induces acute systemic inflammation, potentially affecting patient outcomes.
• This inflammatory response may interact with pre-existing factors like age.
• Previous research often measured limited cytokines, necessitating advanced proteomic approaches for comprehensive analysis.

Purpose of the Study:

• To characterize the acute inflammatory response following TBI using high-dimensional proteomics.
• To differentiate TBI-specific inflammatory markers from general injury responses.
• To correlate inflammatory markers with established TBI biomarkers and neuroimaging outcomes.

Main Methods:

• Plasma samples from 37 TBI, 22 non-TBI trauma, and 28 control participants were analyzed using the Alamar NULISA™ panel (>200 inflammatory markers).
• Inflammatory markers were correlated with plasma NFL, GFAP, tau, UCH-L1, S100B, and MRI measures of lesion volume and white matter injury.
• An Elastic Net model was used to assess 'inflammation age' relative to chronological age.

Main Results:

• Four markers (VSNL1, IL1RN/IL-1Ra, GFAP, IKBKG) were elevated specifically in TBI.
• Higher VSNL1 correlated with increased lesion volume, and higher IL1RN/IL-1Ra with greater white matter injury.
• Elevated IL33 was associated with poorer functional outcomes (GOS-E 1-4). 'Inflammation age' exceeded chronological age in TBI patients.

Conclusions:

• Acute TBI involves both TBI-specific and non-specific inflammatory components.
• These inflammatory markers are linked to structural brain injury and functional outcomes.
• VSNL1, IL1RN/IL-1Ra, and IL33 are potential mediators in TBI pathophysiology, with age modulating the inflammatory response.