A novel human fibroblast growth factor treats experimental intestinal inflammation

Jeffers, Michael; McDonald, William F.; Chillakuru, Rajeev A.; Yang, Meng; Nakase, Hiroshi; Deegler, Lisa L.; Sylander, Elizabeth D.; Rittman, Beth; Bendele, Alison M.; Sartor, R. Balfour; Lichenstein, Henri S.

doi:10.1053/gast.2002.36041

Cited by 64 publications

(43 citation statements)

References 25 publications

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“…EGF has been shown to ameliorate C. difficile toxin-induced mouse enteritis by increasing epithelial cell proliferation (10). A similar effect has been reported for FGF (11,12). The intestinal growth hormone glucagon-like peptide 2 has been shown to reduce mucosal permeability in animal models, such as DSS-induced 3 colitis; similar to the action of EGF, this effect of glucagon-like peptide 2 is associated with the enhancement of mucosal epithelial cell growth (13,14).…”

mentioning

confidence: 59%

“…CopA3 Blocks C. difficile Toxin A-induced Enteritis-EGF and FGF have been shown to inhibit inflammatory responses in the colon by promoting epithelial cell growth, thereby enhancing the physical barrier function (6,12). Because EGF was shown to markedly inhibit the acute enteritis caused by C. difficile toxin A in a mouse model (10), we herein assessed whether CopA3 could also protect against toxin A-induced gut inflammation.…”

Section: Effects Of Copa3 On Epithelial Cell Proliferation and Mucosamentioning

confidence: 99%

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The Insect Peptide CopA3 Increases Colonic Epithelial Cell Proliferation and Mucosal Barrier Function to Prevent Inflammatory Responses in the Gut

Kim

Hwang

Lee

et al. 2016

Journal of Biological Chemistry

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The epithelial cells of the gut form a physical barrier against the luminal contents. The collapse of this barrier causes inflammation, and its therapeutic restoration can protect the gut against inflammation. EGF enhances mucosal barrier function and increases colonocyte proliferation, thereby ameliorating inflammatory responses in the gut. Based on our previous finding that the insect peptide CopA3 promotes neuronal growth, we herein tested whether CopA3 could increase the cell proliferation of colonocytes, enhance mucosal barrier function, and ameliorate gut inflammation. Our results revealed that CopA3 significantly increased epithelial cell proliferation in mouse colonic crypts and also enhanced colonic epithelial barrier function. Moreover, CopA3 treatment ameliorated Clostridium difficile toxin As-induced inflammation responses in the mouse small intestine (acute enteritis) and completely blocked inflammatory responses and subsequent lethality in the dextran sulfate sodium-induced mouse model of chronic colitis. The marked CopA3-induced increase of colonocyte proliferation was found to require rapid protein degradation of p21 Cip1/Waf1 , and an in vitro ubiquitination assay revealed that CopA3 directly facilitated ubiquitin ligase activity against p21 Cip1/Waf1 . Taken together, our findings indicate that the insect peptide CopA3 prevents gut inflammation by increasing epithelial cell proliferation and mucosal barrier function.

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confidence: 59%

Section: Effects Of Copa3 On Epithelial Cell Proliferation and Mucosamentioning

confidence: 99%

The Insect Peptide CopA3 Increases Colonic Epithelial Cell Proliferation and Mucosal Barrier Function to Prevent Inflammatory Responses in the Gut

Kim

Hwang

Lee

et al. 2016

Journal of Biological Chemistry

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“…TABERNERO et al (37) , evaluating the expression of COX-2 in biopsies from patients with intestinal inflammatory disease, detected COX-2 positivity in the arterial wall of all cases, suggesting that this protein possibly exerts a vasoconstrictor effect on the mesenteric arteries of patients with CD. In vitro expression of COX-2 was demonstrated by JEFFERS et al (18) in a study investigating the activity of fibroblast growth factor (FGF) in experimental models, indicating that the therapeutic activity of FGF-20 is a promising candidate for the treatment of intestinal inflammatory disease.…”

Section: A B C Dmentioning

confidence: 99%

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

Romero

Artigiani

Costa

et al. 2008

Arq. Gastroenterol.

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-Background -Crohn's disease accompanied by nonspecific or idiopathic ulcerative proctocolitis corresponds to a condition called intestinal inflammatory disease. The immunoexpression of cyclooxygenase 2 (COX-2) in Crohn's disease becomes more marked with progression of the disease and the presence of wild-type p53 suppresses the transcription of COX-2. Aims -To investigate the immunoexpression of cyclooxygenase 1 (COX-1), COX-2 and p53 in Crohn's ileocolitis and to correlated this expression with clinical and histopathological parameters. Methods -Forty-five cases of Crohn's disease, 16 cases of actinic colitis (diseased-control group) and 11 cases without a history of intestinal disease (normal control group) were studied. Hematoxylin-eosin-stained sections were submitted to histopathological analysis and the immunohistochemical expression of COX-1, COX-2 and p53 was evaluated by the streptavidin-biotin-peroxidase method. Results -Sixty percent of the Crohn's disease patients were women and 40% were men, with 75.5% whites and 25.5% non-whites. The disease involved the terminal ileum in 44.5% of cases, ileum in 33.3%, colon in 20% and duodenum-ileum in 2.2%. A significant association was observed between COX-2 immunoreactivity and age ≤40 years. Histopathological analysis of Crohn's disease samples showed mild or moderate crypt distortion (57.8% and 35.6% of cases), atrophy (6.6%), mild, moderate and marked chronic inflammation (46.7%, 26.7% and 20%), acute inflammatory activity (93.3%), ulceration (24.4%), mucin depletion (37.8%), Paneth's cells (24.4%), intraepithelial lymphocytes (93.3%), and subepithelial collagen (6.7%). In the CD group, COX-1 immunoreactivity in epithelial and inflammatory cells was observed in 26.7% and 22.2% of cases, respectively.

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“…Many agents have been found to have protective effects in the indomethacin-induced enteropathy model which results in relatively milder injury and little lethality. [26][27][28][29][30][31][32] So far, only human glucagon-like peptide 2 has been reported to be protective against indomethacin-induced lethality. 21) We also investigated the effect of OGT on intestinal PGE2 levels.…”

Section: Fig 10 Localization Of Cox-2 Expressing Cellsmentioning

confidence: 99%

An Herbal Medicine Orengedokuto Prevents Indomethacin-Induced Enteropathy

Miura

Fukutake

Yamamoto

et al. 2007

Biological & Pharmaceutical Bulletin

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Prostaglandin E2 (PGE2) is a key regulator of gastrointestinal, immunological, and mucosal homeostasis. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the prostaglandin-producing enzyme cyclooxygenases (COXs), and can induce serious complications, such as gastrointestinal damage, with long-term treatment. Orengedokuto (OGT), a Japanese traditional herbal medicine (Kampo medicine), is effective in various animal models of enteropathy. In the present study we examined whether OGT prevents enteropathy induced by NSAIDs in mice. Ulceration in the small intestine was induced with 2 subcutaneous injections of indomethacin (20 mg/kg body weight). Orally administered OGT prevented or reduced lethality, intestinal lesions, bleeding, increased serum nitrate/nitrite levels, and reduction of mucosal PGE2 induced by indomethacin. These beneficial effects of OGT were accompanied by increased production of PGE2 and interleukin 10 by isolated lamina propria mononuclear cells; COX-2 in these cells may be a major source of PGE2 in normal intestines. These findings suggest that OGT could be an effective therapeutic agent for the treatment of inflammatory bowel disease and adverse reactions to NSAIDs.Key words nonsteroidal anti-inflammatory drug; interleukin 10; herbal medicine; inflammatory bowel disease; prostaglandin E2

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A novel human fibroblast growth factor treats experimental intestinal inflammation

Cited by 64 publications

References 25 publications

The Insect Peptide CopA3 Increases Colonic Epithelial Cell Proliferation and Mucosal Barrier Function to Prevent Inflammatory Responses in the Gut

The Insect Peptide CopA3 Increases Colonic Epithelial Cell Proliferation and Mucosal Barrier Function to Prevent Inflammatory Responses in the Gut

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

An Herbal Medicine Orengedokuto Prevents Indomethacin-Induced Enteropathy

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