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 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.
Calder
P C
PC
School of Medicine, University of Southampton, Southampton SO16 6YD, UK.
Albers
R
R
Antoine
J-M
JM
Blum
S
S
Bourdet-Sicard
R
R
Ferns
G A
GA
Folkerts
G
G
Friedmann
P S
PS
Frost
G S
GS
Guarner
F
F
Løvik
M
M
Macfarlane
S
S
Meyer
P D
PD
M'Rabet
L
L
Serafini
M
M
van Eden
W
W
van Loo
J
J
Vas Dias
W
W
Vidry
S
S
Winklhofer-Roob
B M
BM
Zhao
J
J
D001172:Arthritis, Rheumatoid / Q000178:diet therapy / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000178:diet therapy / Q000503:physiopathology; D002446:Celiac Disease / Q000178:diet therapy / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000178:diet therapy / Q000503:physiopathology*; D015212:Inflammatory Bowel Diseases / Q000178:diet therapy / Q000503:physiopathology; D009747:Nutritional Physiological Phenomena / Q000502:physiology*; D009765:Obesity / Q000178:diet therapy / Q000503:physiopathology; D012130:Respiratory Hypersensitivity / Q000178:diet therapy / Q000503:physiopathology; D012871:Skin Diseases / Q000178:diet therapy / Q000503:physiopathology