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

Abstract

Inhibition of granulocyte activation by surfactant in a 2-yr-old female with meningococcus-induced ARDS. F.K. Tegtmeyer, J.Möller, P. Zabel. #ERS Journals Ltd 2002. 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 a 1 -protease inhibitor (E-a 1 PI) 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-a (TNF-a) and interleukin-6 (IL-6) after endotracheal administration of surfactant (Alveofact1 60 mg?kg?body weight -1 ). In the present case, for the first time, a higher E-a 1 PI 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-a 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.

Deleted in Malignant Brain Tumors 1 (DMBT1) is present in hyaline membranes and modulates surface tension of surfactant

“…The complex of lipids and proteins in pulmonary surfactant enhances pathogen clearance and regulates adaptive and innate immune-cell functions [ 11 ]. Surfactant may decrease immunologic functions as leukocyte activation [ 12 ]. On the other hand, intratracheally administered surfactants may also induce the release of tumor necrosis factor, IL-6 and IL-8 in animal models [ 13 , 14 ].…”

Effects of Positive End-Expiratory Pressure, Inhaled Nitric Oxide and Surfactant on Expression of Proinflammatory Cytokines and Growth Factors in Preterm Piglet Lungs

“…A study performed on isolated and perfused rat lungs seemed to indicate that surfactant was able to induce increased synthesis and release of proinflammatory cytokines (25). In contrast, human studies suggested that surfactant therapy reduced the proinflammatory mediators (26). This differential response to surfactant therapy might be related to the species difference, lung maturation status, and the way of experiment.…”