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Inflammatory disease processes and interactions with nutrition

Inflammatory disease processes and interactions with nutrition
Inflammatory disease processes and interactions with nutrition
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 ?-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 (?-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
inflammation, cytokine, eicosanoid, leucocyte, antioxidant, fatty acid, flavonoids, prebiotic, probiotic
0007-1145
S1-S45
Calder, P.C.
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Albers, R.
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Antoine, J.M.
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Blum, S.
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Bourdet-Sicard, R.
a26da4a1-1c23-4a26-b16a-0947513c962d
Ferns, G.A.
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Folkerts, G.
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Friedmann, P.S.
d50bac23-f3ec-4493-8fa0-fa126cbeba88
Frost, G.S.
b6815962-bb24-40dc-b9a6-45c78c0cfefc
Guarner, F.
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Løvik, M.
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Macfarlane, S.
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Meyer, P.D.
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M'Rabet, L.
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Serafini, M.
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van Eden, W.
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van Loo, J.
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Van Dias, W.
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Vidry, S.
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Winklhofer-Roob, B.M.
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Zhao, J.
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Calder, P.C.
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Albers, R.
63eb3d3b-2052-4ad1-a7aa-888a6781c5e0
Antoine, J.M.
5ba5f978-1140-4f4f-a490-50d88801a4ce
Blum, S.
49c2842a-56b7-47b5-a1ba-2c59ea8f22a9
Bourdet-Sicard, R.
a26da4a1-1c23-4a26-b16a-0947513c962d
Ferns, G.A.
408d2622-347e-42a0-b317-5fc18d7346f8
Folkerts, G.
17764fc8-264a-482c-8d8b-a6860bb93abc
Friedmann, P.S.
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Frost, G.S.
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Guarner, F.
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Løvik, M.
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Macfarlane, S.
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Meyer, P.D.
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M'Rabet, L.
cebbdc31-ed5a-4e43-89fa-ab07dba95b12
Serafini, M.
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van Eden, W.
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van Loo, J.
e4de3f9b-8111-4b18-903b-d042f11ef387
Van Dias, W.
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Vidry, S.
266f4f8e-f16a-4696-847c-828e132fb626
Winklhofer-Roob, B.M.
21b3744f-98ab-4ee8-8640-b29217909ef1
Zhao, J.
5807b9d4-d0e4-4992-a69b-c276636c1691

Calder, P.C., Albers, R., Antoine, J.M., Blum, S., Bourdet-Sicard, R., Ferns, G.A., Folkerts, G., Friedmann, P.S., Frost, G.S., Guarner, F., Løvik, M., Macfarlane, S., Meyer, P.D., M'Rabet, L., Serafini, M., van Eden, W., van Loo, J., Van Dias, W., Vidry, S., Winklhofer-Roob, B.M. and Zhao, J. (2009) Inflammatory disease processes and interactions with nutrition. British Journal of Nutrition, 101 (Supplement S1), S1-S45. (doi:10.1017/S0007114509377867).

Record type: Article

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 ?-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 (?-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

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More information

Published date: May 2009
Keywords: inflammation, cytokine, eicosanoid, leucocyte, antioxidant, fatty acid, flavonoids, prebiotic, probiotic

Identifiers

Local EPrints ID: 147725
URI: http://eprints.soton.ac.uk/id/eprint/147725
ISSN: 0007-1145
PURE UUID: eca0228e-24dc-45ac-95aa-1be0842ed38d
ORCID for P.C. Calder: ORCID iD orcid.org/0000-0002-6038-710X

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Date deposited: 26 Apr 2010 13:03
Last modified: 14 Mar 2024 02:39

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Contributors

Author: P.C. Calder ORCID iD
Author: R. Albers
Author: J.M. Antoine
Author: S. Blum
Author: R. Bourdet-Sicard
Author: G.A. Ferns
Author: G. Folkerts
Author: P.S. Friedmann
Author: G.S. Frost
Author: F. Guarner
Author: M. Løvik
Author: S. Macfarlane
Author: P.D. Meyer
Author: L. M'Rabet
Author: M. Serafini
Author: W. van Eden
Author: J. van Loo
Author: W. Van Dias
Author: S. Vidry
Author: B.M. Winklhofer-Roob
Author: J. Zhao

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