Apoptosis: Implications for inflammatory bowel disease

Levine, Alan D.

doi:10.1002/ibd.3780060307

Cited by 16 publications

(10 citation statements)

References 184 publications

(102 reference statements)

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“…However, IBD patients develop a dysfunction in apoptosis [23–25], that can contribute an increased incidence of colorectal carcinoma, and chemotherapy cytotoxicity of the gut epithelia. Apoptosis can be initiated from cell cycle activation [26–27], cytokine production [28], infective agents [29], or as an adverse response to drugs [30–31].…”

Section: Discussionmentioning

confidence: 99%

Green Tea Polyphenols Mediated Apoptosis in Intestinal Epithelial Cells by a Fadd-Dependent Pathway

Ebersole

2010

JCT

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Colorectal cancer is the most common malignant complication in patients with chronic inflammatory bowel disease (IBD). In addition, these patients are at risk for developing painful complications during chemotherapy due to cytotoxic effects of drugs currently in use. Past studies have suggested a protective effect of tea consumption on gastrointestinal (GI) malignancies. Green tea polyphenols (GrTP) inhibited carcinogen-induced GI tumors in rodents and induced apoptosis in various carcinoma cell lines. We hypothesized that GrTP and its polyphenolic compounds regulate apoptosis in the intestinal epithelia. In this study, the effects of GrTP and its polyphenolics on apoptosis was evaluated in intestinal epithelial, IEC-6, cells grown to 85% confluency. GrTP (400–800 mg/ml) induced DNA fragmentation in a dose dependent fashion. Higher concentrations (>800 mg/ml) induced a mixed apoptosis and cytolysis. Epithelial cells exposed to GrTP and a major polyphenol, EGCG, but not EGC or EC, increased caspase activities in a time and dose dependent manner. The caspase inhibitors rescued cells from GrTP and EGCG-induced cell death. Concomitantly, GrTP resulted in activation of fatty acid synthase (Fas)-associated protein with death domain (FADD) and recruitment to Fas/CD95 domain 30 minutes following treatment. While GrTP also blocked NF-κB activation, an NFκ-B inhibitor (MG132) only promoted cytolysis. In conclusion, these data demonstrated GrTP and EGCG induced apoptosis in intestinal epithelia mediated by caspase-8 through a FADD dependent pathway. Future investigation may warrant preventive as well as therapeutic strategies for GrTP in GI malignancy.

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Section: Discussionmentioning

confidence: 99%

Green Tea Polyphenols Mediated Apoptosis in Intestinal Epithelial Cells by a Fadd-Dependent Pathway

Ebersole

2010

JCT

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“…Apoptosis is a programmed cell death, which under homeostatic conditions exists in harmony with cellular mitosis. Experimental NEC is associated with increased enterocyte apoptosis [12]. We therefore hypothesize that colonization of the intestine by ES may contribute to the pathogenesis of NEC by stimulating release of inflammatory factors and induction of enterocyte apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Enterobacter sakazakiiEnhances Epithelial Cell Injury by Inducing Apoptosis in a Rat Model of Necrotizing Enterocolitis

Hunter¹,

Singamsetty²,

Chokshi³

et al. 2008

J INFECT DIS

108

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SUMMARY Necrotizing enterocolitis (NEC) is an inflammatory intestinal disorder that affects 2–5% of all premature infants. Enterobacter sakazakii (ES), a common contaminant in milk-based powdered infant formula, is implicated as a causative agent of sepsis, meningitis, and NEC in newborn infants with high mortality rates. However, the role of ES in the pathogenesis of NEC is not known to date. Here, we demonstrate for the first time that ES is able to induce clinical and histological NEC in newborn rats. ES was found to bind to enterocytes in rat pups at the tips of villi and to intestinal epithelial cells, IEC-6, in culture with no significant invasion. Exposure to ES induced apoptosis and increased the production of interleukin-6 in IEC-6 cells and in the animal model. These data suggest that ES could be a potential pathogen that induces NEC, and triggers intestinal disease by modulating enterocyte intracellular signaling pathways.

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“…CD represents a T‐helper (Th)1‐mediated condition because mucosal immune cells from affected individuals secrete interferon‐γ and tumor necrosis factor (TNF) as well as interleukin (IL)‐12 and IL‐18, but not Th2‐type cytokines 11. Moreover NF‐κB appears to have an important role in CD,12 and several studies have shown that lamina propria T lymphocytes (LPL) from CD patients, compared with LPL from noninflammatory intestinal mucosa, were significantly less susceptible to apoptosis in response to different pro‐apoptotic stimuli 13,14. In CD, there is an imbalance of the anti‐apoptotic mitochondrial protein Bcl‐2 and the pro‐apoptotic mitochondrial protein Bax14,15 as well as a reduction of caspase 3 activity 16.…”

mentioning

confidence: 99%

Long-standing remission of Crohnʼs disease under imatinib therapy in a patient with Crohnʼs disease

Magro

Costa²

2006

Inflammatory Bowel Diseases

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Apoptosis: Implications for inflammatory bowel disease

Cited by 16 publications

References 184 publications

Green Tea Polyphenols Mediated Apoptosis in Intestinal Epithelial Cells by a Fadd-Dependent Pathway

Green Tea Polyphenols Mediated Apoptosis in Intestinal Epithelial Cells by a Fadd-Dependent Pathway

Enterobacter sakazakiiEnhances Epithelial Cell Injury by Inducing Apoptosis in a Rat Model of Necrotizing Enterocolitis

Long-standing remission of Crohnʼs disease under imatinib therapy in a patient with Crohnʼs disease

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