Modulation of the innate immune response after trauma visualised by a change in functional PMN phenotype.

BACKGROUND: Acute Respiratory Distress Syndrome (ARDS) is a frequent and severe complication after trauma, caused by an excessive inflammatory response mediated by polymorphonuclear granulocytes (PMNs). It was previously demonstrated that patients with activated PMNs in the lungs have PMNs in the peripheral circulation with a reduced active FcgammaRII up-regulating capacity. We tested the hypothesis that a correlation exists between the severity of inflammation and the extent of decreased responsiveness of active FcgammaRII on circulating PMNs, as a sign of altered immunological capacity.
METHODS: Fifty-two patients were included and injury severity was assessed by clinical injury severity scores and base deficit. Symptoms and signs of inflammation were recorded on a daily basis and fMLP-induced active FcgammaRII on PMNs was assessed by FACS analysis within 24h after injury. Results were compared with 10, age matched healthy controls.
RESULTS: The baseline PMN membrane expression of Mac-1/CD11b and active FcgammaRII/CD32 did not correlate with injury severity. Levels of the acute phase protein Interleukin 6 (IL-6) correlated significantly with injury severity, indicating that a range in severity of the inflammatory response was present in the studied population. A statistically significant correlation between the PMN responsiveness towards the bacterial derived peptide fMLP of active FcgammaRII and injury severity was demonstrated. In addition, decreasing responsiveness of active FcgammaRII on PMNs was found in patients who developed systemic inflammatory response syndrome (SIRS) or acute lung injury (ALI)/ARDS.
CONCLUSIONS: The extent of the sustained injury and the subsequent cellular innate immune response is reflected by changes in a functional PMN phenotype of fMLP-induced active FcgammaRII in the peripheral blood.