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Mediators of Inflammation
Volume 3 (1994), Issue 4, Pages 297-302

Cell–Cell Interaction of Macrophages and Vascular Smooth Muscle Cells in the Synthesis of Leukotriene B4

1Laboratoire d'lmmunopharmacologie, Institut des Cordeliers, 15 rue de I'école de Mddecine, Paris 75270, France
2Laboratoire de Biochimie, Hôpital Broussais, Paris 75674, France

Copyright © 1994 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Biosynthesis of LTB4 during cell-cell interaction between vascular smooth muscle cells (SMC) and alveolar macrophages (AM) has been investigated by use of both high-pressure Hquid chromatography (HPLC) and radtoimmunoassay (RIA). Both interleukin-β (IL-β) and tumour necrosis factor-α (TNFα) induced a time- and dose-dependent synthesis of 15-, and 5-hydroxyeicosatetraenoic acids (HETEs) from cultured SMC. However, neither TNFα nor IL-1β induced a significant LTB4 production in SMC alone or AM alone after 24 h of incubation. Addition of IL-1β and TNFα simultaneously to SMC resulted in a dose-dependent synergistic increase of HETEs. Macrophages dose-dependently transformed extremely low concentrations of exogenous LTA4 into LTB4. Incubation of vascular SMC with various numbers of AM in the presence of IL-1β (5 units/ml) and TNFα (10 units/ml) induced a great increase of LTB4 synthesis in comparison with the detectable levels of LTB4 produced by macrophages alone. Pretreatment of SMC with NDGA, cycloheximide, and actinomycin not only inhibited IL-1 and TNT induced HETEs synthesis but also abolished LTB4 production when co-incubated with macrophages. These results suggest that LTB4 in a mixture of SMC and macrophages could originate from a transcellular metabolism, i.e. macrophages transforming SMC-derived LTA4 into LTB4.