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

BackgroundAcute 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 FcγRII up-regulating capacity. We tested the hypothesis that a correlation exists between the severity of inflammation and the extent of decreased responsiveness of active FcγRII on circulating PMNs, as a sign of altered immunological capacity.MethodsFifty-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 FcγRII on PMNs was assessed by FACS analysis within 24 h after injury. Results were compared with 10, age matched healthy controls.ResultsThe baseline PMN membrane expression of Mac-1/CD11b and active FcγRII/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 FcγRII and injury severity was demonstrated. In addition, decreasing responsiveness of active FcγRII on PMNs was found in patients who developed systemic inflammatory response syndrome (SIRS) or acute lung injury (ALI)/ARDS.ConclusionsThe 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 FcγRII in the peripheral blood.