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- W2077803778 abstract "Macrophage (MØ)-mediated fibrin deposition via induction of procoagulant activity (PCA) is an important component of the host response during various infections. While endotoxin (LPS) is a well-known stimulus of PCA, the factors modulating its activity within the inflammatory microenvironment are unknown. The purpose of these studies was to determine the relative roles of two pathways of arachidonic acid metabolism, i.e., the cyclooxygenase (CO) and 5-lipoxygenase (5-LO) pathways, in modulating MØ PCA induction by LPS. Thioglycolate-elicited murine peritoneal MØ were treated with the CO inhibitor indomethacin (INDO), the 5-LO inhibitor nordihydroguaiaretic acid (NDGA), or control vehicle for 15 min prior to a 4-hr exposure to LPS (10 μg/ml). The ability of MØ to shorten the clotting time of plasma (i.e., PCA) was measured and clotting times were converted to PCA units via a thromboplastin standard. While CO blockade had no effect on PCA induction by LPS (without INDO 30 μM 446 ± 131, with INDO 30 μM 546 ± 193, mU/2 × 106 cells, n = 4), NDGA caused a dose-dependent inhibition (IC50 = 3 μM) without affecting cell viability (without NDGA 3 μM 446 ± 131, with NDGA 3 μM 191 ± 67, mU/2 × 106 cells, n = 6, P < 0.05). Induction of PCA by Escherichia coli was similarly inhibited (E. coli 106 alone = 518 ± 130; with NDGA 3 μM = 234 ± 100, n = 2). Combined NDGA/INDO reduced PCA comparable to NDGA alone, ruling out the possibility that NDGA acted through generation of inhibitory prostanoids like PGE2. Thus, 5-LO products appear to contribute to the induction of MØ-mediated fibrin deposition by gram-negative bacteria and their surface components. This suggests a novel approach to modulating the local inflammatory response." @default.
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- W2077803778 date "1992-06-01" @default.
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- W2077803778 title "Modulation of macrophage procoagulant activity by arachidonic acid metabolites" @default.
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- W2077803778 doi "https://doi.org/10.1016/0022-4804(92)90127-l" @default.
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