PMID- 8726941 OWN - NLM STAT- MEDLINE DCOM- 19961122 LR - 20190821 IS - 0903-1936 (Print) IS - 0903-1936 (Linking) VI - 9 IP - 4 DP - 1996 Apr TI - In vitro modulation of induced neutrophil activation by different surfactant preparations. PG - 752-7 AB - Endotracheal surfactant administration has gained an important role in the treatment of respiratory failure. Polymorphonuclear neutrophil granulocyte (PMN) activation mediated by chemoattractants, such as interleukin-8 (IL-8), neutrophil-activating peptide-2 (NAP-2) and formylated bacterial oligopeptides, has been found to be involved in the pathophysiology of acute respiratory failure. We investigated potential modulating effects of commercial surfactant preparations (Exosurf, Alveofact, Curosurf and Survanta) on spontaneous and chemoattractant-induced PMN function. Isolated cytochalasin B (CytB)-treated PMNs from healthy adults were incubated with increasing concentrations of surfactant. The response of the cells was measured in terms of elastase release from the lysosomes within 30 min. The PMNs showed no direct activation by any of the surfactants tested. However, when cells were stimulated with suboptimal dosages of chemokines, such as IL-8 (2 nM) or NAP-2 (100 nM), or formyl-methionyl-leucyl-phenylalanine (fMLP) (50 nM), and co-incubated with increasing concentrations of surfactant (0.05-8 mg.mL-1) the release of elastase was markedly modulated depending on the surfactant preparation used. Whilst Exosurf and Alveofact showed only modest effects on the elastase release induced by all three mediators, Curosurf and Survanta markedly inhibited the cellular response in a dose-dependent manner. At concentrations above 1 mg.mL-1, Curosurf and Survanta decreased the IL-8-, NAP-2- and fMLP-induced elastase release by 83, 67 and 90%, and by 82, 75 and 80%, respectively. In conclusion, exogenous surfactant may modulate the inflammatory response of the airways by affecting the chemoattractant-induced polymorphonuclear neutrophil activation. Surfactant preparations with inhibiting properties on neutrophil activation may participate in the prevention of neutrophil-induced lung damage. FAU - Tegtmeyer, F K AU - Tegtmeyer FK AD - Children's Hospital, Park Schonfeld, Kassel, FRG. FAU - Gortner, L AU - Gortner L FAU - Ludwig, A AU - Ludwig A FAU - Brandt, E AU - Brandt E LA - eng PT - Journal Article PL - England TA - Eur Respir J JT - The European respiratory journal JID - 8803460 RN - 0 (Interleukin-8) RN - 0 (PPBP protein, human) RN - 0 (Peptides) RN - 0 (Surface-Active Agents) RN - 0 (beta-Thromboglobulin) RN - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine) RN - 69344-77-0 (connective tissue-activating peptide) RN - EC 3.4.21.37 (Leukocyte Elastase) SB - IM MH - Adult MH - Cells, Cultured MH - Humans MH - Interleukin-8/immunology MH - Leukocyte Elastase/metabolism MH - Lysosomes/enzymology MH - N-Formylmethionine Leucyl-Phenylalanine/immunology MH - Neutrophil Activation/*drug effects MH - Neutrophils/chemistry/enzymology MH - Peptides/immunology MH - Surface-Active Agents/*pharmacology MH - beta-Thromboglobulin EDAT- 1996/04/01 00:00 MHDA- 1996/04/01 00:01 CRDT- 1996/04/01 00:00 PHST- 1996/04/01 00:00 [pubmed] PHST- 1996/04/01 00:01 [medline] PHST- 1996/04/01 00:00 [entrez] AID - 10.1183/09031936.96.09040752 [doi] PST - ppublish SO - Eur Respir J. 1996 Apr;9(4):752-7. doi: 10.1183/09031936.96.09040752.