Early Immune Alterations in Adult Patients with Trauma According to Injury Severity: Cell-Death Patterns and Inflammatory Mediator Profiles.

Background/

Objectives

Trauma triggers complex early immune responses. However, the relationship among trauma severity, changes in immune cell survival, and circulating inflammatory mediators remains unclear. This study compared early cell viability and death patterns in CD66b+ granulocytes, total T lymphocytes, and CD4+ and CD8+ T-cell subsets as well as inflammatory mediator levels between patients with non-severe and severe trauma.

Methods

This single-center prospective observational study included 67 adult patients with trauma who were classified into non-severe and severe trauma groups according to the Injury Severity Score (ISS < 15 vs. ISS ≥ 15). Blood samples were obtained within 1 h of arrival at the emergency department. Flow cytometry was used to assess the viability, early apoptosis, late apoptosis, and necrosis in the leukocyte subsets. Serum concentrations of intercellular adhesion molecule-1 (ICAM-1), macrophage migration inhibitory factor (MIF), CD40 ligand (CD40L), and interleukin-1 receptor antagonist (IL-1ra) were measured using enzyme-linked immunosorbent assays.

Results

The severe trauma group had a significantly lower proportion of early apoptotic CD66b+ granulocytes than the non-severe trauma group (2.9% [1.4-6.7] vs. 6.3% [3.7-10.9], p = 0.001), whereas the live, late apoptotic, and necrotic CD66b+ granulocyte fractions did not differ significantly between the two groups. Most T-cell death parameters were similar between the groups, although an exploratory increase in necrotic CD4+ T lymphocyte abundance was observed in the severe trauma group. IL-1ra levels were significantly higher in the severe trauma group than in the non-severe trauma group and were associated with ISS in both mediator-only and adjusted sensitivity regression analyses.

Conclusions

Severe trauma was associated with reduced early apoptosis in the CD66b+ granulocyte compartment and elevated IL-1ra levels shortly after injury compared with non-severe trauma. These findings suggest that early immune alterations after severe trauma may involve compartment-specific granulocyte death patterns and counter-regulatory inflammatory responses rather than generalized changes across leukocyte populations.