Suppression of the neutrophil chemiluminescence response in blood of multiply traumatized patients with and without the adult respiratory distress syndrome (ARDS)

Conclusions

From the results, alterations of humoral and cellular components of the nonspecific immune system were supposed to be involved in the ARDS pathogenesis. Concerning the intravascular compartment, a plasma opsonin defect could be observed, especially for group C patients with a later EVLW increase. Furthermore, these patients demonstrated a continuous synthesis of a trauma factor that suppressed CL responses and presumably also phagocytosis/killing functions of PMNL in blood, hereby predisposing this patient group to sepsis and sepsis-amplified ARDS development. Such an inhibition factor has been described by Lanser et al. [5] in septic patients, but our results demonstrated that this factor seemed always to be synthetized after a traumatic event irrespective of septicemia. As a consequence, the increased endogenous respiratory burst potential of neutrophils, especially of patients with a later EVLW increase, becomes effective after the neutrophil has left the capillary and entered the alveolar space, no longer being kept in check by the trauma factor and then liberating the complete set of inflammation mediators for lung structure damage.