- Poster presentation
- Open Access
Effects of recombinant surfactant protein C and elastase inhibitor on neutrophil apoptosis
© BioMed Central Ltd. 2004
- Published: 15 March 2004
- Acute Lung Injury
- Acute Respiratory Distress Syndrome
- Density Gradient Centrifugation
- Polymorphonuclear Leukocyte
- Neutrophil Elastase
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are associated with mortality in excess of 50%. About 5–35% of patients with sepsis develop ARDS and the condition is characterised by infiltration and accumulation of activated polymorphonuclear leukocytes (PMNL) within the capillary and alveolar spaces. Increased alveolar neutrophil elastase and decreased antiprotease activity also occurs. Elastase directly damages surfactant-specific protein in vitro and alters surfactant function. Recombinant surfactant protein C (r-SPC) improves pulmonary dynamics, oxygenation and reduces hyaline membrane formation in animal models of ALI/ARDS. Accumulated neutrophils are removed by programmed cell death or apoptosis, resulting in resolution and healing. We determined the effect of r-SPC with and without elastase inhibitor (EI) on neutrophil apoptosis.
P value (Wilcoxon signed ranks)
LPS + r-SPC
LPS + EI
LPS + r-SPC + EI
The results of this pilot study show that r-SPC significantly increases activated PMNL apoptosis, and this is maintained in the presence of EI. This suggests the possible use of r-SPC and elastase inhibitor in inducing neutrophil apoptosis and hence clearance of neutrophils in ALI/ARDS. Further studies are needed.