Journal of Leukocyte Biology
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© 2003 by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1202601

Received for publication December 10, 2002.
Revised February 26, 2003.
Accepted for publication February 27, 2003.

Article

Regulation of platelet-activating factor synthesis in human monocytes by dipalmitoyl phosphatidylcholine

Amanda J. Tonks *, Alex Tonks *@, Roger H. K. Morris {dagger}, Kenneth P. Jones {dagger}, and Simon K. Jackson {ddagger}

Departments of *Haematology and {ddagger}Medical Microbiology, University of Wales College of Medicine, Cardiff, United Kingdom; and {dagger}School of Applied Science, University of Wales Institute Cardiff, United Kingdom

@ To whom correspondence should be addressed. E-mail: priceaj1{at}cf.ac.uk.


  Abstract

Platelet-activating factor (PAF) has a major role in inflammatory responses within the lung. This study investigates the effect of pulmonary surfactant on the synthesis of PAF in human monocytic cells. The pulmonary surfactant preparation Curosurf® significantly inhibited lipopolysaccharide (LPS)-stimulated PAF biosynthesis (P<0.01) in a human monocytic cell line, Mono mac-6 (MM6), as determined by 3H PAF scintillation-proximity assay. The inhibitory properties of surfactant were determined to be associated, at least in part, with the 1,2-dipalmitoyl phosphatidylcholine (DPPC) component of surfactant. DPPC alone also inhibited LPS-stimulated PAF biosynthesis in human peripheral blood monocytes. DPPC treatment did not affect LPS-stimulated phospholipase A2 activity in MM6 cell lysates. However, DPPC significantly inhibited LPS-stimulated coenzyme A (CoA)-independent transacylase and acetyl CoA:lyso-PAF acetyltransferase activity. DPPC treatment of MM6 cells decreased plasma membrane fluidity as demonstrated by electron paramagnetic resonance spectroscopy coupled with spin labeling. Taken together, these findings indicate that pulmonary surfactant, particularly the DPPC component, can inhibit LPS-stimulated PAF production via perturbation of the cell membrane, which inhibits the activity of specific membrane-associated enzymes involved in PAF biosynthesis.

Key Words: inflammation • lung • lipid • immune modulation




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