Metabolic interactions between eicosanoids in blood and vascular cells

Lagarde, Michel; Gualde, N.; Rigaud, M.

doi:10.1042/bj2570313

Cited by 50 publications

(14 citation statements)

References 117 publications

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“…One cannot be sure that blocking COX-2 by NS-398 inhibits only PGE 2 synthesis and does not weakly affect other PG production. However, our former assessment using gas chromatography and mass spectrometry showed that immune cells, among them APC, produce mostly PGE 2 and that synthesis of other COX-issued eicosanoids (PGs, prostacyclin, thromboxane) is quite weak (65).…”

Section: Discussionmentioning

confidence: 90%

Cyclooxygenase-2-Issued Prostaglandin E2 Enhances the Production of Endogenous IL-10, Which Down-Regulates Dendritic Cell Functions

Harizi

Juzan

Pitard

et al. 2002

The Journal of Immunology

351

287

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PGE2 is a well-known immunomodulator produced in the immune response by APCs, such as dendritic cells (DCs), the most potent APC of the immune system. We investigated the PGE2 biosynthetic capacity of bone marrow-derived DC (BM-DC) and the effects of PG on the APC. We observed that BM-DC produce PGE2 and other proinflammatory mediators, such as leukotriene B4 and NO, after LPS exposure. Constitutively present in BM-DC, cyclooxygenase (COX)-1 did not contribute significantly to the total pool of PGE2 compared with the LPS-induced COX-2-produced PGE2. Treatment of BM-DC with exogenous PGE2 induced the production of large amounts of IL-10 and less IL-12p70. In addition, selective inhibition of COX-2, but not COX-1, was followed by significant decrements in PGE2 and IL-10, a concomitant restoration of IL-12 production, and an enhancement of DC stimulatory potential. In contrast, we found no demonstrable role for leukotriene B4 or NO. In view of the potential of PGE2 to stimulate IL-10, we examined the possibility that the suppressive effect of PGE2 is mediated via IL-10. We found that exogenous IL-10 inhibits IL-12p70 production in the presence of NS-398, a COX-2 selective inhibitor, while the inhibitory effects of PGE2 were totally reversed by anti-IL-10. We conclude that COX-2-mediated PGE2 up-regulates IL-10, which down-regulates IL-12 production and the APC function of BM-DC.

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Section: Discussionmentioning

confidence: 90%

Cyclooxygenase-2-Issued Prostaglandin E2 Enhances the Production of Endogenous IL-10, Which Down-Regulates Dendritic Cell Functions

Harizi

Juzan

Pitard

et al. 2002

The Journal of Immunology

351

287

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“…Singling out the direct endothelial damage by radiation as a primary event is not supported either by the common knowledge that, whereas the microvasculature may be affected, the major blood vessels are mostly spared. Within the narrower scope of this part of the review which focuses on bioactive arachidonic acid dcrivatives, the possibility of blood vessel changes after irradiation being regulatory in character and caused at least in part indirectly (i.e., mediated by diffusible species also generated in nonvascular cells) is further supported by studies on heterologous cell-cell interactions in eicosanoid synthesis (66)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77)(78)(79). There seems therefore to be insufficient reason for investigating only the endothelium and vascular smooth muscle cells in an attempt to unravel radiationinduced changes in blood vessels; responses of the intervening (i.e., other stromal and parenchymal) and bloodcirculating cells, as well as reciprocal cell interactions must be taken into account.…”

Section: -10 Gymentioning

confidence: 99%

On Radiation Damage to Normal Tissues and its Treatment: II. Anti-inflammatory drugs

Michałowski

1994

Acta Oncologica

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“…Via a transcellular mechanism, LTA 4 produced in neutrophils may be transformed by platelets into sulphidopeptide leucotrienes (LTC 4 , LTD 4 and LTE 4 ) (Pace‐Asciak et al , 1986; Maclouf & Murphy, 1988) and lipoxins (Serhan et al , 1984; Conti et al , 1990). On the other hand, 5,12‐diHETE may be formed in activated platelets by the action of 12‐LOX on 5‐HETE released from neutrophils (Lagarde et al , 1989). It could be then argued that the decreased production of LTB 4 was due to the transcellular metabolism of LTA 4 and 5‐HETE respectively.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of AA metabolism in platelets may stimulate the 5‐LOX activity in neutrophils (Maclouf et al , 1982). On the other hand, some AA metabolites produced in neutrophils may be transferred to platelets, or vice versa , leading to the formation of other metabolites not generated by either cell type alone (Marcus et al , 1982; Lagarde et al , 1989). It is known that 5S,12S‐dihydroxyeicosatetraenoic acid (5,12‐diHETE) can be formed by activated platelets through the action of 12‐lipoxygenase on 5‐HETE released from neutrophils (Maclouf & Murphy, 1988).…”

mentioning

confidence: 99%

Platelets may inhibit leucotriene biosynthesis by human neutrophils at the integrin level

et al. 2003

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Summary. Polymorphonuclear leucocytes and blood platelets co-operate in several pathophysiological processes, and arachidonic acid (AA) metabolites produced in response to the activation of these cells are potent mediators of their functions. We studied the role of platelets in the formation of 5-lipoxygenase products from AA by autologous neutrophils, especially the chemotactic agent leucotriene (LT) B 4 . The formation of all products, namely 5-hydroxy-eicosatetraenoic acid (5-HETE), LTB 4 and the other LTA 4 -derived metabolites, in response to the calcium ionophore A23187 was evaluated by high-performance liquid chromatography. All the 5-lipoxygenase products were significantly diminished by physiological concentrations of platelets. This inhibitory effect was lost when platelets were previously degranulated by thrombin in non-aggregating conditions. Peptides containing the Arg-Gly-Asp-Ser or His-His-Leu-Gly-Gly-Ala-Lys-Gln-AlaGly-Asp-Val sequence, which prevent the adhesion of platelets to neutrophils via the fibrinogen released from platelet granules and the integrin glycoprotein IIb/IIIa, markedly decreased the inhibitory effect of non-degranulated platelets. The production of transcellular metabolites of AA such as LTC 4 , the dual 5-and 12-lipoxygenase product 5,12-diHETE and lipoxins could not account for the decreased formation of 5-HETE and LTA 4 -derived metabolites. It is concluded that platelets may inhibit the neutrophil 5-lipoxygenase activity at the integrin level and in turn may play a role in slowing down the production of LTB 4 in the course of inflammation.

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Metabolic interactions between eicosanoids in blood and vascular cells

Cited by 50 publications

References 117 publications

Cyclooxygenase-2-Issued Prostaglandin E2 Enhances the Production of Endogenous IL-10, Which Down-Regulates Dendritic Cell Functions

Cyclooxygenase-2-Issued Prostaglandin E2 Enhances the Production of Endogenous IL-10, Which Down-Regulates Dendritic Cell Functions

On Radiation Damage to Normal Tissues and its Treatment: II. Anti-inflammatory drugs

Platelets may inhibit leucotriene biosynthesis by human neutrophils at the integrin level

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