Tumor necrosis factor α-producing cells in the intestinal mucosa of children with inflammatory bowel disease

Breese, Emma J.; Michie, Colin; Nicholls, S.; Murch, Simon; Williams, Christopher; Domizio, Paola; Walker-Smith, J A; MacDonald, Thomas T.

doi:10.1016/0016-5085(94)90398-0

Cited by 533 publications

(274 citation statements)

References 45 publications

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“…Two common features of IBD involve increased cytokine production (26,27) and increased apoptosis of intestinal cells (28). We have reported that a central cytokine in the pathogenesis of IBD, tumor necrosis factor (TNF) (27), regulates both anti-and pro-apoptotic signaling pathways, and the balance between these two kinds of signals determines the cell fate (29).…”

mentioning

confidence: 99%

Probiotic Bacterium Prevents Cytokine-induced Apoptosis in Intestinal Epithelial Cells

Yan

Polk

2002

Journal of Biological Chemistry

472

328

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Probiotic bacteria are microorganisms that benefit the host by preventing or ameliorating disease. However, little information is known regarding the scientific rationale for using probiotics as alternative medicine. The purpose of this paper is to investigate the mechanisms of probiotic beneficial effects on intestinal cell homeostasis. We now report that one such probiotic, Lactobacillus rhamnosus GG (LGG), prevents cytokineinduced apoptosis in two different intestinal epithelial cell models. Culture of LGG with either mouse or human colon cells activates the anti-apoptotic Akt/protein kinase B. This model probiotic also inhibits activation of the pro-apoptotic p38/mitogen-activated protein kinase by tumor necrosis factor, interleukin-1␣, or ␥-interferon. Furthermore, products recovered from LGG culture broth supernatant show concentration-dependent activation of Akt and inhibition of cytokine-induced apoptosis. These observations suggest a novel mechanism of communication between probiotic microorganisms and epithelia that increases survival of intestinal cells normally found in an environment of pro-apoptotic cytokines.

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mentioning

confidence: 99%

Probiotic Bacterium Prevents Cytokine-induced Apoptosis in Intestinal Epithelial Cells

Yan

Polk

2002

Journal of Biological Chemistry

472

328

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“…6,7 Hence, it was of interest to determine whether this proinflammatory cytokine could induce ID1 in endothelial cells. TNF-a caused dose-dependent induction of ID1 mRNA in both human umbilical vein endothelial cells and human intestinal microvascular endothelial cells (Figure 4, A and B).…”

Section: Id1 and Endothelial Cellsmentioning

confidence: 99%

Id1 Expression in Endothelial Cells of the Colon Is Required for Normal Response to Injury

Zhang

Subbaramaiah

Yantiss

et al. 2015

The American Journal of Pathology

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Inhibitor of DNA binding (ID)-1 is important for angiogenesis during embryogenesis and tumor development. Whether ID1 expression in endothelial cells of the colon is required for normal response to injury is unknown. We demonstrate that Id1 is up-regulated in colonic endothelial cells in an experimental model of colitis and in the inflamed mucosa of patients with inflammatory bowel disease. Because prostaglandin E 2 and tumor necrosis factor-a are also elevated in colitis, we determined whether these factors could induce ID1 transcription in cultured endothelial cells. Tumor necrosis factor-a stimulated ID1 transcription via early growth response 1 protein (Egr-1). By contrast, the induction of ID1 by prostaglandin E 2 was mediated by cAMP response elementebinding protein (CREB). To determine whether the increased ID1 levels in the endothelial cells of inflamed mucosa were an adaptive response that modulated the severity of tissue injury, Id1 was conditionally depleted in the endothelium of mice, which sensitized the mice to more severe chemical colitis, including more severe diarrhea, bleeding, and histological injury, and shorter colon compared with control mice. Moreover, depletion of Id1 in the vasculature was associated with increased CD31 þ aggregates and increased vascular permeability in inflamed mucosa compared with those in Id1 wild-type control mice. These results suggest that endothelial ID1 up-regulation in inflamed colonic mucosa is an adaptive response that modulates the severity of tissue injury. (Am J Pathol 2015 http://dx

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“…Although cytokine profiles differ for CD and UC with CD associated with a Th1-type response whereas UC is associated with a Th2 type response, TNF-a is implicated in both disorders (reviewed in [21]). Indeed, serum and stool TNF-a concentrations and the frequency of TNF-a-secreting mononuclear cells are higher in IBD patients than in healthy controls [22][23][24]. Kontoyiannis et al [25] reported that dysregulation of TNF-a expression in mice induces Crohn's-like IBD and chronic inflammatory arthritis.…”

Section: Tnf-a In Gastrointestinal Diseasesmentioning

confidence: 99%

How the Discovery of TNF-α Has Advanced Gastrointestinal Diseases and Treatment Regimes

St‐Pierre

Chadee

2014

Dig Dis Sci

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Tumor necrosis factor α-producing cells in the intestinal mucosa of children with inflammatory bowel disease

Cited by 533 publications

References 45 publications

Probiotic Bacterium Prevents Cytokine-induced Apoptosis in Intestinal Epithelial Cells

Probiotic Bacterium Prevents Cytokine-induced Apoptosis in Intestinal Epithelial Cells

Id1 Expression in Endothelial Cells of the Colon Is Required for Normal Response to Injury

How the Discovery of TNF-α Has Advanced Gastrointestinal Diseases and Treatment Regimes

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