Histidine – a naturally occurring amino acid – found to inhibit NF-kB
An elemental diet is limited to basic nutrients in liquid form. No protein is included in the diet. Individual amino acids, the building blocks of proteins, are provided instead.
An elemental diet has found to be effective in Crohn’s disease, but for unknown reasons.
The authors of the study below investigated the role of histidine – an amino acid – in relieving colitis. They found that histidine reduced NF-kB activation in macrophages. Another amino acid, alanine, had no such effect.
The publication:
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Gastroenterology. 2009 Feb;136(2):564-74.e2. Epub 2008 Oct 7.
Dietary histidine ameliorates murine colitis by inhibition of proinflammatory cytokine production from macrophages.
Andou A, Hisamatsu T, Okamoto S, Chinen H, Kamada N, Kobayashi T, Hashimoto M, Okutsu T, Shimbo K, Takeda T, Matsumoto H, Sato A, Ohtsu H, Suzuki M, Hibi T.
Summary of the abstract
BACKGROUND & AIMS: Elemental diet (ED) is effective for human Crohn’s disease (CD).
Although some of this effectiveness may be due to its low antigenic load and low fat content, the mechanisms remain unclear.
We sought to assess the role of histidine, one of the constituent amino acids of ED, in controlling colitis.
METHODS: The interleukin (IL)-10-deficient (IL-10(-/-)) cell transfer model of colitis was used.
RESULTS: In the IL-10(-/-) transfer model, dietary histidine, but not alanine, reduced histologic damage and colon weight and TNF-alpha mRNA expression.
Histidine inhibited LPS-induced TNF-alpha and IL-6 production by mouse macrophages in a concentration-dependent manner, whereas alanine or histidine-related metabolites had no such effect.
Histidine inhibited LPS-induced NF-kappaB in macrophages.
CONCLUSIONS: These results showed that histidine could be a novel therapeutic agent for CD by inhibition of NF-kappaB activation, following down-regulation of proinflammatory cytokine production by macrophages. Thus, our studies provided new insights into the roles of amino acid metabolism in the pathophysiology of CD and for therapeutic strategies.
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