Cell–Cell Interaction of Macrophages and Vascular Smooth Muscle Cells in the Synthesis of Leukotriene B4
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...
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| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S0962935194000414 |
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| Summary: | 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. |
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| ISSN: | 0962-9351 1466-1861 |