Role of Cytokines and Platelet-Activating Factor in Microvascular Immune Injury

Braquet, P.; Hosford, David; Braquet, M.; Bourgain, R.H.; Bussolino, Federico

doi:10.1159/000234755

Cited by 102 publications

(43 citation statements)

References 16 publications

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“…PAF has been shown to induce vascular inflammation and vasculitis in experimental animals [7,8]. It has also been implicated in asthma [9], and may play a role in the initiation and progression of atherosclerosis [10].…”

Section: Introductionmentioning

confidence: 99%

Induction of IL-4 by platelet-activating factor

Huang

Elinder

Owman

et al. 1996

Clinical and Experimental Immunology

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SUMMARYPlatelet-activating factor (PAF) is a phospholipid inflammatory mediator which is synthesized by a variety of cells, including monocytes, endothelial cells, mast cells and neutrophils. PAF acts via a recently cloned PAF receptor, present on monocytes and endothelial cells, but not on non-activated lymphocytes. IL-4 is mainly produced by T lymphocytes, and belongs to the Th2 subset of T helper cells. IL-6 is mainly a monocyte/macrophage-derived cytokine with multiple proinflammatory effects. We here report that PAF induces IL-4 production, as determined by ELISPOT. Antibodies to MHC class II inhibited the IL-4 stimulatory effects of PAF. PAF also had the capacity to induce IgA production, as determined by ELISPOT, and IL-6 production in peripheral blood mononuclear cells (PBMC) as determined by ELISA. These PAF-mediated effects were completely inhibited by a specific PAFreceptor antagonist, WEB 2170. Taken together, our data indicate that PAF activates T lymphocytes to IL-4 production by an indirect, monocyte-dependent mechanism dependent on MHC class II. PAF also enhances antibody formation and IL-6 production from PBMC. These findings indicate that PAF activates immune-competent cells, which may be of importance in inflammatory diseases such as asthma, vasculitis and atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

Induction of IL-4 by platelet-activating factor

Huang

Elinder

Owman

et al. 1996

Clinical and Experimental Immunology

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“…1,2 Hypercholesterolemia could increase the release of plateletactivating factor (PAF), 2 which in turn could increase the synthesis and release of interleukin-1 4 and tumor necrosis factor. 5 Leukotriene B 4 , 6 PAF, 7 interleukin-1, 8 and tumor necrosis factor 9 are known to stimulate PMNLs to produce OFRs, which would initiate the development of hypercholesterolemic atherosclerosis.…”

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confidence: 99%

Reduction of Serum Cholesterol and Hypercholesterolemic Atherosclerosis in Rabbits by Secoisolariciresinol Diglucoside Isolated From Flaxseed

1999

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Background-Secoisolariciresinol diglucoside (SDG) is a plant lignan isolated from flaxseed. Lignans are plateletactivating factor-receptor antagonists that would inhibit the production of oxygen radicals by polymorphonuclear leukocytes. SDG is an antioxidant. Antioxidants studied thus far are known to reduce hypercholesterolemic atherosclerosis. The objective of this study was to determine the effect of SDG on various blood lipid and aortic tissue oxidative stress parameters and on the development of atherosclerosis in rabbits fed a high-cholesterol diet. Methods and Results-Rabbits were assigned to 4 groups: group 1, control; group 2, SDG control (15 mg ⅐ kg body wt Ϫ1 ⅐ d Ϫ1 PO); group 3, 1% cholesterol diet; and group 4, same as group 3 but with added SDG (15 mg ⅐ kg body wt Ϫ1 ⅐ d

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“…Interestingly, endothelial injury activates complement (C 3 and C 5 ) (Webster et al 1980). Activated complement, platelet-activating factor (PAF), leukotrienes B 4 (LTB 4 ) and TNF stimulate PMNLs to release oxygen free radicals (Ford-Hutchinson et al 1980;Braquet et al 1989;Zoratti et al 1991;Paubert-Braquet et al 1988). This evidence suggests that there could be increased OR production contributing to the genesis of atherosclerosis.…”

Section: Oxygen Radicals and Atherosclerosismentioning

confidence: 99%

Homocysteine and Malondialdehyde as Predictors of Restenosis Following Percutaneous Coronary Intervention

et al. 2006

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Restenosis is one of the major adverse outcomes of Percutaneous CoronaryIntervention (PCI). Previous studies have shown conflicting reports for homocysteine as a predictor of restenosis following PCI. The conflicting reports may be due to oxidative factors (stimulation of polymorphonuclear leukocyte [PMNL]-induced reactive oxygen species generation, xanthine-xanthine oxidase, and arachidonic acid metabolism) other than homocysteine which could cause endothelial cell dysfunction leading to restenosis.Malondialdehyde (MDA), a lipid peroxidation product, is a marker for oxidative stress and is related to all oxidative factors. Therefore, it is possible that serum MDA may be a better predictor of restenosis than plasma homocysteine. The purpose of this study is to determine whether or not the pre-procedural serum MDA and plasma homocysteine levels are elevated in patients who develop restenosis post PCI.The study included fifty-one patients undergoing elective PCI who consented to participate in a protocol that was approved by the Ethics Committee of the University of Saskatchewan. Homocysteine and malondialdehyde were measured in the plasma and serum respectively. Blood samples were collected pre-procedural, 0 time, 8 hours, 24 hours, and 6 months post-procedure. Exercise tolerance tests were performed at two weeks, and six months post-procedure to determine if there was any evidence of restenosis.The results of the study showed that pre-procedural values of plasma homocysteine in the restenosis and non-restenosis groups were 10.37 ± 0.46 and 10.73 ± 0.49 respectively. These values were not significantly different (p=0.60) between the groups. The pre-procedural levels of plasma homocysteine were not significantly ii different (p=0.08) from the post-PCI values of those patients who did not develop restenosis at the 6-month time interval. However, the pre-procedural levels of plasma homocysteine were significantly different from the post-PCI values of those patients in the restenosis group at the 24hr (p=0.04) and 6-month (p=0.002) time intervals. In the restenosis group there was a significant increase (24%) after six months in the values of homocysteine from the pre-procedural levels. Thus, this indicates that restenosis is associated with higher post-PCI levels of homocysteine.The pre-procedural levels of serum MDA in the restenosis and non-restenosis groups were 0.124± 0.16 and 0.147± 0.02 respectively. There was no significant difference (p=0.60) between the two groups. There was also no significant difference The results suggest that pre-procedural levels of plasma homocysteine and serum MDA were not predictors of restenosis following PCI. However, the post-PCI sixmonth levels of both homocysteine and MDA are predictors of restenosis. Moreover, the post-PCI levels of MDA were better predictors of restenosis than the post-PCI levels of homocysteine because the increase in MDA levels were greater at six months than the rise in homocysteine levels at the same time interval.iii ACKNOWLEDGEMENTS

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Role of Cytokines and Platelet-Activating Factor in Microvascular Immune Injury

Cited by 102 publications

References 16 publications

Induction of IL-4 by platelet-activating factor

Induction of IL-4 by platelet-activating factor

Reduction of Serum Cholesterol and Hypercholesterolemic Atherosclerosis in Rabbits by Secoisolariciresinol Diglucoside Isolated From Flaxseed

Homocysteine and Malondialdehyde as Predictors of Restenosis Following Percutaneous Coronary Intervention

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