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Inhibition of granulocyte activation by surfactant in a 2-yr-old female with meningococcus-induced ARDS

¹ Children's Hospital "Park Schönfeld", Kassel, ² Dept of Paediatrics, Medical University of Lübeck, Lübeck, and ³ Dept of Immunology and Cell Biology, "Forschungszentrum Borstel", Borstel, Germany

CORRESPONDENCE: F.K. Tegtmeyer, Kinderkrankenhaus Park Schönfeld, Frankfurter Str. 167, 34121, Kassel, Germany. Fax: 49 5619285220. E-mail: fk.Tegtmeyer@park-schoenfeld.de

Keywords: acute respiratory distress syndrome, elastase, interleukin-6, neutrophil granulocytes, surfactant, tumour necrosis factor-

Received: July 6, 2001
Accepted September 7, 2001

Abstract

Activated polymorphonuclear neutrophils (PMNs) play a crucial role in acute respiratory distress syndrome (ARDS) via extracellular release of reactive cell products such as elastase. Surfactant has proved valuable in restoring lung function in ARDS. The significance of its immunomodulatory properties with respect to this effect has not yet been clarified. The aim of the present study was to determine the anti-inflammatory effects of surfactant administration in an infant with ARDS.

During the acute phase of ARDS in a 2-yr-old female, levels of PMN-derived elastase complexed with ₁-protease inhibitor (E-₁PI) were measured in both arterial and central venous blood samples obtained simultaneously. The results were correlated with oxygen demand and plasma concentrations of tumour necrosis factor- (TNF-) and interleukin-6 (IL-6) after endotracheal administration of surfactant (Alveofact® 60 mg·kg·body weight^–1).

In the present case, for the first time, a higher E-₁PI concentration was detected in arterial blood (4.51 mg·L^–1) than in central venous blood (2.28 mg·L^–1). After administration of surfactant, these concentrations and the arteriovenous difference decreased, indicating that during ARDS, most PMN degranulation takes place in the pulmonary vascular bed and is inhibited by surfactant administration. Simultaneously, TNF- and IL-6 plasma concentrations decreased within hours and lung function was restored.

This local inhibition of polymorphonuclear neutrophil activation by exogenous surfactant may play a key role in the early improvement in lung function after surfactant administration.