Regulating inflammation through the anti-inflammatory enzyme platelet-activating factor-acetylhydrolase

Neto, Hugo C. Castro Faria; Stafforini, Diana M.; Prescott, Stephen M.; Zimmerman, Guy A.

doi:10.1590/s0074-02762005000900014

Cited by 45 publications

(17 citation statements)

References 83 publications

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“…PAF‐like oxidized phospholipids are oxidatively modified phospholipids that can be produced by oxidative stress. Plasma PAF‐AH plays an anti‐inflammatory role by hydrolysing PAF and PAF‐like oxidized phospholipids, which are potent pro‐inflammatory mediators . However, the role of this enzyme in atherosclerosis is controversial because the hydrolysis products of this enzyme, lysophosphatidylcholine and oxidatively modified nonesterified fatty acids, can promote the pathogenesis of atherosclerosis ; thus, controversy remains regarding whether plasma PAF‐AH exerts a pro‐ or anti‐inflammatory action.…”

Section: Discussionmentioning

confidence: 99%

Activity and distribution of plasma platelet‐activating factor acetylhydrolase in women with gestational diabetes mellitus and their neonates

Gao

Zhang

et al. 2016

Diabetes Metabolism Res

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Section: Discussionmentioning

confidence: 99%

Activity and distribution of plasma platelet‐activating factor acetylhydrolase in women with gestational diabetes mellitus and their neonates

Gao

Zhang

et al. 2016

Diabetes Metabolism Res

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“…2 PAF has been shown to exert its effects at concentrations as low as 10 212 mol/L, 22,30 with a half-life of approximately 3 to 13 minutes, depending on the time to inactivation by PAF-AH. 22,[30][31][32] PAF and PAF-AH levels have been shown to be inversely correlated in studies of anaphylaxis, demonstrating more severe clinical symptoms with higher PAF levels. 33 Since its discovery, our knowledge surrounding the role of PAF has expanded to include its effects on platelet aggregation and its role as a vasodilator and bronchoconstrictor, its role in host defense, and its role as a mediator of the inflammatory response (Table III).…”

Section: Biological Effects Of Pafmentioning

confidence: 99%

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Gill

Jindal

Jagdis

et al. 2015

Journal of Allergy and Clinical Immunology

109

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Anaphylaxis is an acute, severe, life-threatening multisystem allergic reaction resulting from the sudden systemic release of biochemical mediators and chemotactic substances. Release of both preformed granule-associated mediators and newly generated lipid-derived mediators contributes to the amplification and prolongation of anaphylaxis. Platelet-activating factor (PAF) is a potent phospholipid-derived mediator the central role of which has been well established in experimental models of both immune-mediated and non-immune mediated anaphylaxis. It is produced and secreted by several types of cells, including mast cells, monocytes, tissue macrophages, platelets, eosinophils, endothelial cells, and neutrophils. PAF is implicated in platelet aggregation and activation through release of vasoactive amines in the inflammatory response, resulting in increased vascular permeability, circulatory collapse, decreased cardiac output, and various other biological effects. PAF is rapidly hydrolyzed and degraded to an inactive metabolite, lysoPAF, by the enzyme PAF acetylhydrolase, the activity of which has shown to correlate inversely with PAF levels and predispose to severe anaphylaxis. In addition to its role in anaphylaxis, PAF has also been implicated as a mediator in both allergic and nonallergic inflammatory diseases, including allergic rhinitis, sepsis, atherosclerotic disease, and malignancy, in which PAF signaling has an established role. The therapeutic role of PAF antagonism has been investigated for several diseases, with variable results thus far. Further investigation of its role in pathology and therapeutic modulation is highly anticipated because of the pressing need for more selective and targeted therapy for the management of severe anaphylaxis.

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“…Monocytes, thus activated, render inflammatory-thrombotic responses and aggregation. Plasma PAF acetylhydrolase may terminate the triggered signals by hydrolyzing PAF-like substances generated in a milieu of enhanced inflammation/oxidant stress [71].…”

Section: Systemic Inflammation Autoimmune Activation and Hdl Dysfunctionmentioning

confidence: 99%

Type-2 diabetes and coronary heart disease: common physiopathology, viewed from autoimmunity

Onat¹,

Dönmez²,

Karadeniz³

et al. 2014

Expert Review of Cardiovascular Therapy

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Two highly prevalent diseases, Type-2 diabetes mellitus and coronary heart disease (CHD), share risk factors. Excess levels of LDL-cholesterol have been overemphasized to uniformly encompass the development of CHD, and the origin of insulin resistance underlying Type-2 diabetes has not been fully elucidated. Autoimmune response has been recognized to be responsible only of a small minority of diabetes. The increasing trend in the worldwide prevalence of diabetes and the risk factors for both diseases are reviewed, the independent mediation for CHD of (central) adiposity in both diseases and the 'hypertriglyceridemic waist' phenotype are outlined. Evidence is described that serum lipoprotein (Lp)(a) concentrations, not only in excess, but also in apparently 'reduced' levels, as a result of autoimmune response, underlie both disorders and are closely related to insulin resistance.

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Regulating inflammation through the anti-inflammatory enzyme platelet-activating factor-acetylhydrolase

Abstract: Platelet-activating factor (PAF) is one of the most potent lipid mediators involved in inflammatory events

Cited by 45 publications

References 83 publications

Activity and distribution of plasma platelet‐activating factor acetylhydrolase in women with gestational diabetes mellitus and their neonates

Activity and distribution of plasma platelet‐activating factor acetylhydrolase in women with gestational diabetes mellitus and their neonates

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Type-2 diabetes and coronary heart disease: common physiopathology, viewed from autoimmunity

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