Dietary Histidine Ameliorates Murine Colitis by Inhibition of Proinflammatory Cytokine Production From Macrophages

Andou, Ayatoshi; Hisamatsu, Tadakazu; Okamoto, Susumu; Chinen, Hiroshi; Kamada, Nobuhiko; Hashimoto, Masaki; Okutsu, Tomohisa; Shimbo, Kazutaka; Takeda, Tomoko; Matsui, Hideki; Satō, Atsushi; Ohtsu, Hiroshi; Suzuki, Manabu; Hibi, Toshifumi

doi:10.1053/j.gastro.2008.09.062

Cited by 148 publications

(120 citation statements)

References 34 publications

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“…8). The anti-inflammatory activity of histidine was confirmed in an animal experiment by Andou et al 93) using IL-10 knock-out mice. Methionine also inhibited IL-8 secretion in Caco-2 cells induced by H 2 O 2 , TNF-, and IL-1.…”

Section: Food Substances That Suppress Chemokine Secretion From Iecsmentioning

confidence: 80%

Interaction between Food Substances and the Intestinal Epithelium

Shimizu

2010

Bioscience, Biotechnology, and Biochemistry

129

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The small intestine is an organ responsible for nutrient absorption, barrier functions, signal recognition/transduction, and the production of bioactive compounds. These functions are known to be regulated by such factors as hormones and cytokines, but substances contained in the daily diet are also thought to play roles as major modulators of intestinal functions. Intestinal epithelial cells (IECs), which form a monolayer covering the inside surface of the intestinal tract, are particularly important in this modulation, because they directly interact with intestinal contents, including food substances, their digests, and gut microbial components. Using cell-based in vitro assays, we investigated the food-IEC interactions at the cellular and molecular levels, and found that a variety of food substances affected the transporter activity, tight junction permeability, metabolic enzyme expression, immune functions, and so on. Modulation of the intestinal functions by dietary substances is therefore essential to promote health.

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Section: Food Substances That Suppress Chemokine Secretion From Iecsmentioning

confidence: 80%

Interaction between Food Substances and the Intestinal Epithelium

Shimizu

2010

Bioscience, Biotechnology, and Biochemistry

129

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“…Although the meaning of the change in each pathway is not clear, a significant decrease in the proportion of histidine metabolism was commonly observed in CD and UC patients. Andou et al previously demonstrated that oral administration of histidine ameliorated intestinal inflammation in interleukin-10-deficient mice [39]. Reduced histidine metabolism in the gut microbiome in IBD patients might therefore be involved in the development of mucosal inflammation.…”

Section: Discussionmentioning

confidence: 98%

Analysis of endoscopic brush samples identified mucosa-associated dysbiosis in inflammatory bowel disease

et al. 2017

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Background The mucosa-associated gut microbiota directly modulates epithelial and mucosal function. In this study, we investigated the mucosa-associated microbial community in patients with inflammatory bowel disease (IBD), using endoscopic brush samples. Methods A total of 174 mucus samples from 43 patients with ulcerative colitis (UC), 26 with Crohn's disease (CD) and 14 non-IBD controls were obtained by gentle brushing of mucosal surfaces using endoscopic cytology brushes. The gut microbiome was analyzed using 16S rRNA gene sequencing. Results There were no significant differences in microbial structure among different anatomical sites (the ileum, cecum and sigmoid colon) within individuals. There was, however, a significant difference in microbial structure between CD, UC and non-IBD controls. The difference between CD and non-IBD controls was more marked than that between UC patients and non-IBD controls. a-Diversity was significantly lower in UC and CD patients than non-IBD controls. When comparing CD patients with non-IBD controls, the phylum Proteobacteria was significantly increased and the phyla Firmicutes and Bacteroidetes were significantly reduced. These included a significant increase in the genera Escherichia, Ruminococcus (R. gnavus), Cetobacterium, Actinobacillus and Enterococcus, and a significant decrease in the genera Faecalibacterium, Coprococcus, Prevotella and Roseburia. Comparisons between CD and UC patients revealed a greater abundance of the genera Escherichia, Ruminococcus (R. gnavus), Clostridium, Cetobacterium, Peptostreptococcus in CD patients, and the genera Faecalibacterium, Blautia, Bifidobacterium, Roseburia and Citrobacter in UC patients. Conclusions Mucosa-associated dysbiosis was identified in IBD patients. CD and UC may be distinguishable from the mucosa-associated microbial community structure.

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“…33) and dendritic cells, the 2 major cellular sources of elevated IL-6 levels in chronic inflammation-associated carcinogenesis (31). To evaluate whether epimorphin deletion inhibits IL-6 secretion from other cell types, we examined the effect of epimorphin deletion on resident peritoneal macrophages, which are reflective of the intestinal environment and well-described in the colitis model (34,35), and on bone marrow-derived dendritic cells. Resident peritoneal macrophages were cultured as described previously (35,36), and supernatants were collected for IL-6 assay.…”

Section: Figurementioning

confidence: 99%

Epimorphin deletion protects mice from inflammation-induced colon carcinogenesis and alters stem cell niche myofibroblast secretion

Shaker¹,

Swietlicki²,

Wang³

et al. 2010

J. Clin. Invest.

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Epithelial-mesenchymal interactions regulate normal gut epithelial homeostasis and have a putative role in inflammatory bowel disease and colon cancer pathogenesis. Epimorphin is a mesenchymal and myofibroblast protein with antiproliferative, promorphogenic effects in intestinal epithelium. We previously showed that deletion of epimorphin partially protects mice from acute colitis, associated with an increase in crypt cell proliferation. Here we explored the potential therapeutic utility of modulating epimorphin expression by examining the effects of epimorphin deletion on chronic inflammation-associated colon carcinogenesis using the azoxymethane/dextran sodium sulfate (AOM/DSS) model. We found that mice in which epimorphin expression was absent had a marked reduction in incidence and extent of colonic dysplasia. Furthermore, epimorphin deletion in myofibroblasts altered the morphology and growth of cocultured epithelial cells. Loss of epimorphin affected secretion of soluble mesenchymal regulators of the stem cell niche such as Chordin. Importantly, IL-6 secretion from LPS-treated epimorphin-deficient myofibroblasts was completely inhibited, and stromal IL-6 expression was reduced in vivo. Taken together, these data show that epimorphin deletion inhibits chronic inflammation-associated colon carcinogenesis in mice, likely as a result of increased epithelial repair, decreased myofibroblast IL-6 secretion, and diminished IL-6-induced inflammation. Furthermore, we believe that modulation of epimorphin expression may have therapeutic benefits in appropriate clinical settings.

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Dietary Histidine Ameliorates Murine Colitis by Inhibition of Proinflammatory Cytokine Production From Macrophages

Cited by 148 publications

References 34 publications

Interaction between Food Substances and the Intestinal Epithelium

Interaction between Food Substances and the Intestinal Epithelium

Analysis of endoscopic brush samples identified mucosa-associated dysbiosis in inflammatory bowel disease

Epimorphin deletion protects mice from inflammation-induced colon carcinogenesis and alters stem cell niche myofibroblast secretion

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