Pro-Inflammatory Inhibition


ScFOS & Inulin Fermentation Products:         Anaerobic fermentation of scFOS and oligofructose-enriched inulin by bacteria in the colon gives rise to three major short chain fatty acids (SCFA) namely acetic, propionic and butyric. The anti-inflammatory effect of the latter has been well documented in the literature but is exemplified in a study involving colonic biopsy specimens obtained from inflamed and/or non-inflamed mucosa of patients with active or inactive Crohn’s Disease. Biopsies were cultured with or without butyrate (2 and 10 mM) and assayed for TNFα. The results showed that biopsies from inflamed mucosa produced higher levels of TNFα than those from non-inflamed or normal mucosa. In the presence of butyrate, TNFα levels were decreased dose dependently in both inflamed and non-inflamed biopsies. The authors concluded that butyrate decreases proinflammatory cytokine expression via inhibition of NF-κB activation and IκBα degradation and that these anti-inflammatory properties provide a rationale for assessing butyrate in the treatment of CD. In an in vitro investigation[1], the authors demonstrated that acetate and propionate possessed anti-inflammatory properties comparable to those of butyrate. The study involved SCFA inhibition of lipopolysaccharide (LPS)-induced TNFα release from human blood-derived neutrophils. The results (see image below) show that all three SCFA are effective in inhibiting TNFα release with propionic and butyric more active than acetic. The authors concluded that propionate and acetate, in addition to butyrate, could be useful in the treatment of inflammatory disorders, including IBD.


EGCG: In this study[2], the authors examined the anti-inflammatory effects of EGCG on LPS-mediated TNFα release from a macrophage cell line. The results showed that EGCG induced a significant decrease in TNFα protein levels in a dose-response fashion (see image below). The authors conclude that the anti-inflammatory mechanism of green tea polyphenols is mediated at least in part through down-regulation of TNFα gene expression by blocking NF-κB activation. The authors further suggest that green tea polyphenols may be effective therapy for a variety of inflammatory processes. Interestingly, EGCG at higher doses caused a modest increase in TNFα and this effect is attributed to EGCG transformation to hydrogen peroxide[3] and a pro-oxidant effect.




Green tea Polyphenols (>95%):   In this animal study[4], the authors used interleukin-2-deficient mice (C57BL/6J, an autoimmunity model) to evaluate the role of green tea polyphenols in treating chronic inflammatory states, such as inflammatory bowel disease. The mice were daily supplemented with water containing 1% sugar (Control) or 1% sugar containing 0.5% GTP for 1 week, humanely killed and their colons excised for examination of cytokines TNFα and INFγ. The results demonstrated significant reduction in the GTP group compared to control (image below).


 The authors conclude that theirs was the first study to to demonstrate the benefits of green tea in an animal model of spontaneous chronic inflammation and IBD, especially incorporating the diet when the disease was well established. They further comment that this approach is more in line with the use of therapies during the active phase of the disease and further supports the use of green tea polyphenols in the treatment of inflammatory diseases.


[1] Tedelind S et al (2007) Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: A study with relevance to inflammatory bowel disease. World Journal of Gastroenterology 13(20):2826-2832.
[2] Yang F et al (1998) Green tea polyphenols block endotoxin-induced tumor necrosis factor-production and lethality in a murine model. Journal of Nutrition 128:2334-2340.
[3] Arakawa H et al (2004) Role of hydrogen peroxide in bactericidal action of catechin. Biological & Pharmaceutical Bulletin 27(3):277-281.
[4] Varilek GW et al (2001) Green tea polyphenol extract attenuates inflammation in interleukin-2-deficient mice, a model of autoimmunity. Journal of Nutrition 131:2034-2039.

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