Inflammatory disease processes and interactions with nutrition
Philip C. Calder,Ruud Albers,Jean-Michel Antoine,Stephanie Blum,Raphaëlle Bourdet-Sicard,Gordon A. Ferns,Gert Folkerts,Peter S. Friedmann,Gary Frost,Francisco Guarner,M. Løvik,S. Macfarlane,P. D. Meyer,Laura M'rabet,Mauro Serafini,W. van Eden,J. van Loo,W. Vas Dias,S. Vidry,Brigitte M. Winklhofer-Roob,J. Zhao +20 more
TLDR
Dietary components including long chain ω-3 fatty acids, antioxidant vitamins, plant flavonoids, prebiotics and probiotics have the potential to modulate predisposition to chronic inflammatory conditions and may have a role in their therapy.Abstract:
Inflammation is a stereotypical physiological response to infections and tissue injury; it initiates pathogen killing as well as tissue repair processes and helps to restore homeostasis at infected or damaged sites. Acute inflammatory reactions are usually self-limiting and resolve rapidly, due to the involvement of negative feedback mechanisms. Thus, regulated inflammatory responses are essential to remain healthy and maintain homeostasis. However, inflammatory responses that fail to regulate themselves can become chronic and contribute to the perpetuation and progression of disease. Characteristics typical of chronic inflammatory responses underlying the pathophysiology of several disorders include loss of barrier function, responsiveness to a normally benign stimulus, infiltration of inflammatory cells into compartments where they are not normally found in such high numbers, and overproduction of oxidants, cytokines, chemokines, eicosanoids and matrix metalloproteinases. The levels of these mediators amplify the inflammatory response, are destructive and contribute to the clinical symptoms. Various dietary components including long chain omega-3 fatty acids, antioxidant vitamins, plant flavonoids, prebiotics and probiotics have the potential to modulate predisposition to chronic inflammatory conditions and may have a role in their therapy. These components act through a variety of mechanisms including decreasing inflammatory mediator production through effects on cell signaling and gene expression (omega-3 fatty acids, vitamin E, plant flavonoids), reducing the production of damaging oxidants (vitamin E and other antioxidants), and promoting gut barrier function and anti-inflammatory responses (prebiotics and probiotics). However, in general really strong evidence of benefit to human health through anti-inflammatory actions is lacking for most of these dietary components. Thus, further studies addressing efficacy in humans linked to studies providing greater understanding of the mechanisms of action involved are required.read more
Citations
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Dietary (Poly)phenolics in Human Health: Structures, Bioavailability, and Evidence of Protective Effects Against Chronic Diseases
Daniele Del Rio,Ana Rodriguez-Mateos,Jeremy P. E. Spencer,Massimiliano Tognolini,Gina Borges,Alan Crozier +5 more
TL;DR: It is concluded that better performed in vivo intervention and in vitro mechanistic studies are needed to fully understand how (poly)phenol molecules interact with human physiological and pathological processes.
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Marine omega-3 fatty acids and inflammatory processes: Effects, mechanisms and clinical relevance
TL;DR: Mechanisms underlying the anti-inflammatory actions of marine n-3 fatty acids include altered cell membrane phospholipid fatty acid composition, disruption of lipid rafts, and inhibition of activation of the pro-inflammatory transcription factor nuclear factor kappa B so reducing expression of inflammatory genes.
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Association of the adam33 gene with asthma and bronchial hyperresponsiveness
TL;DR: The identification and characterization of ADAM33, a putative asthma susceptibility gene identified by positional cloning in an outbred population, should provide insights into the pathogenesis and natural history of this common disease.
Journal ArticleDOI
Dietary factors and low-grade inflammation in relation to overweight and obesity
Philip C. Calder,Namanjeet Ahluwalia,Fred Brouns,Timo Buetler,Karine Clément,Karen Cunningham,Katherine Esposito,Lena S. Jönsson,Hubert Kolb,Mirian Lansink,Ascensión Marcos,Andrew N. Margioris,Nathan V. Matusheski,Herve Nordmann,John O’Brien,Giuseppe Pugliese,Salwa W. Rizkalla,Casper G. Schalkwijk,Jaakko Tuomilehto,Julia Wärnberg,Bernhard Watzl,Brigitte M. Winklhofer-Roob +21 more
TL;DR: Potential mechanisms are described and research gaps, which limit the understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified.
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