Inflammatory cytokine mRNA in monocytes is modified by a recombinant (SP-C)-based surfactant and porcine surfactant.

Respiratory distress syndrome (RDS) is mainly caused by a deficiency of surfactant in structurally immature lungs. Therapy for RDS consists of mechanical ventilation and administration of exogenous surfactant. Animal-derived surfactant preparations that are used to treat newborn infants show inhibition of proinflammatory cytokines. There are no data available concerning the effects of the new generation of surfactants. In the present study, the effects of an animal-derived surfactant (Curosurf) and a synthetic surfactant (Venticute) on lipopolysaccharide (LPS)-induced inflammation were tested in human monocyte THP-1 cells. The effects were measured as changes in messenger RNA (mRNA) expression of the chemokine interleukin-8 (IL-8), proinflammatory TNF-alpha and the anti-inflammatory IL-10 cytokine. Both surfactant preparations inhibited the LPS-induced increase in TNF-alpha expression. A comparison of both preparations revealed a similar effect on IL-10 expression. However, IL-10 expression was higher after incubation with Venticute. Curosurf increased IL-8 expression at higher concentrations, but Venticute had no effect. The anti-inflammatory effect of an animal-derived surfactant and a new-generation synthetic surfactant preparation may influence postnatal pulmonary inflammation.
AuthorsAndreas Wemhöner, Mario Rüdiger, Ludwig Gortner
JournalMethods and findings in experimental and clinical pharmacology (Methods Find Exp Clin Pharmacol) Vol. 31 Issue 5 Pg. 317-23 (Jun 2009) ISSN: 0379-0355 [Print] Spain
PMID19649338 (Publication Type: Journal Article)
CopyrightCopyright 2009 Prous Science, S.A.U. or its licensors. All rights reserved.
Chemical References
  • Biological Products
  • Cytokines
  • Interleukin-8
  • Lipopolysaccharides
  • Phospholipids
  • RNA, Messenger
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Venticute
  • Interleukin-10
  • poractant alfa
  • Biological Products (pharmacology)
  • Cells, Cultured
  • Cytokines (genetics)
  • Humans
  • Interleukin-10 (biosynthesis)
  • Interleukin-8 (genetics)
  • Lipopolysaccharides (pharmacology)
  • Monocytes (metabolism)
  • Phospholipids (pharmacology)
  • RNA, Messenger (analysis)
  • Recombinant Proteins (pharmacology)
  • Tumor Necrosis Factor-alpha (genetics)

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