Histidine inhibits colitis inflammation

[Kofi]

I've started supplementing with histidine years ago when my metabolic
panel came back indicating a severe deficiency.

Gastroenterology. 2009 Feb;136(2):564-74.e2. Epub 2008 Oct 7.
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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.
Department of Internal Medicine, School of Medicine, Keio University,
Tokyo, Japan.

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.
SCID mice with colitis induced by transfer of IL-10(-/-) cells were
maintained on experimented diets containing either single amino acids or
a mixture. The severity of colitis was assessed by wet colon weight.
Colonic tumor necrosis factor (TNF)-alpha messenger RNA (mRNA)
expression was detected by quantitative reverse-transcription polymerase
chain reaction. Mouse peritoneal macrophages were stimulated by
lipopolysaccharides (LPS), with or without amino acids. The
concentration of cytokines in the supernatant was determined by
enzyme-linked immunosorbent assay. Inhibitor of nuclear factor
(NF)-kappaB-alpha and nuclear p65 were confirmed by immunoblotting.
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.

Publication Types:
* Research Support, Non-U.S. Gov't

PMID: 19027739