The Effect of Egg Yolk in Diets on Anaphylactic Arthritis (Passive Arthus Phenomenon) in the Guinea Pig

Coburn, Alvin F.; Graham, Claire E.; Haninger, Joan

doi:10.1084/jem.100.5.425

Cited by 66 publications

(39 citation statements)

References 4 publications

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“…Indeed, the anti-inflammatory properties of PEA were first described over fifty years ago (Coburn et al, 1954) and are well established Costa et al, 2002;De Petrocellis et al, 2001;Di Marzo et al, 2001b;Lo Verme et al, 2005a;Mazzari et al, 1996;Re et al,2007). PEA does not bind to CB 1 or CB 2 receptors (Di Marzo et al, 2001b;Lambert and Di Marzo, 1999;Lambert et al, 2002), however, SR144528 has been found to block the anti-edema effects of PEA that is administered before carrageenan Lichtman et al, 2004;Malan et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of fatty acid amides in the carrageenan-induced paw edema model

et al. 2008

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While it has long been recognized that Δ 9 -tetrahydrocannabinol (THC), the primary psychoactive constituent of cannabis, and other cannabinoid receptor agonists possess anti-inflammatory properties, their well known CNS effects have dampened enthusiasm for therapeutic development. On the other hand, genetic deletion of fatty acid amide hydrolase (FAAH), the enzyme responsible for degradation of fatty acid amides, including endogenous cannabinoid N-arachidonoyl ethanolamine (anandamide; AEA), N-palmitoyl ethanolamine (PEA), N-oleoyl ethanolamine (OEA), and oleamide, also elicits anti-edema, but does not produce any apparent cannabinoid effects. The purpose of the present study was to investigate whether exogenous administration of FAAs would augment the anti-inflammatory phenotype of FAAH (-/-) mice in the carrageenan model. Thus, we evaluated the effects of the FAAs AEA, PEA, OEA, and oleamide in wild-type and FAAH (-/-) mice. For comparison, we evaluated the anti-edema effects of THC, dexamethasone (DEX), a synthetic glucocorticoid, diclofenac (DIC), a nonselective cyclooxygenase (COX) inhibitor, in both genotypes. A final study determined if tolerance to the anti-edema effects of PEA occurs after repeated dosing. PEA, THC, DEX, DIC elicited significant decreases in carrageenan-induced paw edema in wild type mice. In contrast OEA produced a less reliable anti-edema effect than these other drugs, and AEA and oleamide failed to produce any significant decreases in paw edema. Moreover, none of the agents evaluated augmented the anti-edema phenotype of FAAH (-/-) mice, suggesting that maximal antiedema effects had already been established. PEA was the most effective FAA in preventing paw edema and its effects did not undergo tolerance. While the present findings do not support a role for AEA in preventing carrageenan-induced edema, PEA administration and FAAH blockade elicited anti-edema effects of an equivalent magnitude as produced by THC, DEX, and DIC in this assay.

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Section: Discussionmentioning

confidence: 99%

Evaluation of fatty acid amides in the carrageenan-induced paw edema model

et al. 2008

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“…The potential benefit of FAEs first came to the light in 1943 when Coburn & Moore [141] reported on the antipyretic properties of dried chicken egg yolk in children with rheumatic fever. A decade later, this same group identified the lipid fraction from egg yolk as the component responsible for this effect [142], with PEA being the active component [143]. The therapeutic applications of this lipid amide remained largely overlooked, however, until the emerging characterization of its antiinflammatory [144], analgesic [145] and anti-convulsant [146] properties.…”

Section: Microglia and Mast Cells As Therapeutic Targetsmentioning

confidence: 99%

Mast cell–glia axis in neuroinflammation and therapeutic potential of the anandamide congener palmitoylethanolamide

Skaper

Facci

2012

Phil. Trans. R. Soc. B

101

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Communication between the immune and nervous systems depends a great deal on pro-inflammatory cytokines. Both astroglia and microglia, in particular, constitute an important source of inflammatory mediators and may have fundamental roles in central nervous system (CNS) disorders from neuropathic pain and epilepsy to neurodegenerative diseases. Glial cells respond also to pro-inflammatory signals released from cells of immune origin. In this context, mast cells are of particular relevance. These immune-related cells, while resident in the CNS, are able to cross a compromised bloodspinal cord and blood-brain barrier in cases of CNS pathology. Emerging evidence suggests the possibility of mast cell-glia communication, and opens exciting new perspectives for designing therapies to target neuroinflammation by differentially modulating the activation of non-neuronal cells normally controlling neuronal sensitization-both peripherally and centrally. This review aims to provide an overview of recent progress relating to the pathobiology of neuroinflammation, the role of glia, neuro-immune interactions involving mast cells and the possibility that glia-mast cell interactions contribute to exacerbation of acute symptoms of chronic neurodegenerative disease and accelerated disease progression, as well as promotion of pain transmission pathways. Using this background as a starting point for discussion, we will consider the therapeutic potential of naturally occurring fatty acid ethanolamides, such as palmitoylethanolamide in treating systemic inflammation or blockade of signalling pathways from the periphery to the brain in such settings.

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“…In a continuation of this research, it was demonstrated that lipid fractions purified from egg yolk (Coburn et al, 1954;Long and Martin, 1956), as well as peanut oil and soybean lecithin (Long and Miles, 1950), exerted anti-allergic effects in the guinea pig (see Fig. 2 for a timeline of events).…”

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confidence: 99%

The search for the palmitoylethanolamide receptor

et al. 2005

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Palmitoylethanolamide (PEA), the naturally occurring amide of ethanolamine and palmitic acid, is an endogenous lipid that modulates pain and inflammation. Although the anti-inflammatory effects of PEA were first characterized nearly 50 years ago, the identity of the receptor mediating these actions has long remained elusive. We recently identified the ligand-activated transcription factor, peroxisome proliferator-activated receptor-alpha (PPAR-a), as the receptor mediating the anti-inflammatory actions of this lipid amide. Here we outline the history of PEA, starting with its initial discovery in the 1950s, and discuss the pharmacological properties of this compound, particularly in regards to its ability to activate PPAR-a. Discovery of PEAThe discovery of naturally occurring fatty acid ethanolamides (FAEs) (Fig. 1) stems from an interesting clinical finding in the early 1940s, when investigators noted that supplementing the diets of 0024-3205/$ -see front matter D

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The Effect of Egg Yolk in Diets on Anaphylactic Arthritis (Passive Arthus Phenomenon) in the Guinea Pig

Cited by 66 publications

References 4 publications

Evaluation of fatty acid amides in the carrageenan-induced paw edema model

Evaluation of fatty acid amides in the carrageenan-induced paw edema model

Mast cell–glia axis in neuroinflammation and therapeutic potential of the anandamide congener palmitoylethanolamide

The search for the palmitoylethanolamide receptor

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