Nuclear factor κB is activated in macrophages and epithelial cells of inflamed intestinal mucosa

Rogler, Gerhard; Brand, Korbinian; Vogl, Daniela; Page, Sharon; Hofmeister, Robert; Andus, Tilo; Knuechel, Ruth; Baeuerle, Patrick A.; Schölmerich, Jürgen; Groß, Volker

doi:10.1016/s0016-5085(98)70202-1

Cited by 669 publications

(483 citation statements)

References 41 publications

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“…The molecular mechanisms involved in the suppressive effects of flavonoids on NF-jB are currently unknown, but several possibilities have been postulated. Flavonoids may inhibit NF-jB by acting as antioxidants, since NF-jB is a redox-sensitive transcription factor and activated by oxidant stress in the inflamed intestinal mucosa [36]. However, again this is pointed out in this work due to the fact that although quercitrin retained its antioxidant potential, it was unable to modulate NF-jB activation in the in vitro experiments.…”

Section: Discussionmentioning

confidence: 62%

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

et al. 2005

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Quercetin is a common antioxidant flavonoid found in vegetables, which is usually present in glycosylated forms, such as quercitrin (3-rhamnosylquercetin). Previous in vitro experiments have shown that quercetin exerts a bigger effect than quercitrin in the down-regulation of the inflammatory response. However, such results have not been reproduced in in vivo experimental models of intestinal inflammation, in which quercetin did not show beneficial effects while its glycosides, quercitrin or rutin, have demonstrated their effectiveness. In this study, we have reported that the in vivo effects of quercitrin in the experimental model of rat colitis induced by dextran sulfate sodium can be mediated by the release of quercetin generated after glycoside's cleavage by the intestinal microbiota. This is supported by the fact that quercetin, but not quercitrin, is able to down-regulate the inflammatory response of bone marrow-derived macrophages in vitro. Moreover, we have demonstrated that quercetin inhibits cytokine and inducible nitric oxide synthase expression through inhibition of the NF-jB pathway without modification of c-Jun N-terminal kinase activity (both in vitro and in vivo). As a conclusion, our report suggests that quercitrin releases quercetin in order to perform its anti-inflammatory effect which is mediated through the inhibition of the NF-jB pathway.

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Section: Discussionmentioning

confidence: 62%

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

et al. 2005

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“…We show that immunoreactivity of these two molecules is also seen in macrophages in colonic polyps. The same anti active NF-kB antibody has been used to perform immunohistochemistry in formalin ®xed, para n embedded tissue in other studies including several that have shown activated NF-kB in macrophages (Gaweco et al, 2000;Rogler et al, 1998). We ourselves have previously shown the speci®city of this antibody under the same conditions by showing colocalisation of TNFa, TRAF-2 and total NF-kB staining with the active NF-kB staining and showing clear nuclear localisation of the active NF-kB (van Den Brink et al, 2000).…”

Section: Discussionmentioning

confidence: 91%

NF-kappaB, p38 MAPK and JNK are highly expressed and active in the stroma of human colonic adenomatous polyps

et al. 2001

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The factors that govern the progression from colonic adenomatous polyp to colon cancer are poorly understood. The observation that NSAIDs act as chemopreventative agents and reduce the size of colonic polyps suggests the involvement of in¯ammatory signalling, but in¯ammatory signalling in colonic polyps has not been studied. We investigated the expression of the active forms of NF-kB, JNK and p38 MAPK using immunohistochemistry with activation speci®c antibodies in human colonic adenomas. We show that active NF-kB is seen in stromal macrophages that also express COX-2 and TNF-a, active JNK is seen in stromal and intraepithelial T-lymphocytes and periendothelial cells of new blood vessels, and active p38 MAPK is most highly expressed in macrophages and other stromal cells. These results demonstrate the presence of active in¯ammatory signal transduction in colonic polyps and that these are predominantly in the stroma. In the case of NF-kB this coincides with the cellular localisation of COX-2. These results support evidence that NSAIDs may act through e ects on stromal cells rather than epithelial cells. Oncogene (2001) 20, 819 ± 827.

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“…Because we hypothesized that PHB may exert positive feedback regulation on itself, we next addressed whether sustained expression of PHB would diminish the effects of TNF-␣ on NF-B activation, which is increased during intestinal inflammation (Rogler et al, 1998) and mediates TNF-␣-induced decrease in PHB expression. We therefore measured NF-B activation in PHB overexpressing cells compared with cells overexpressing vector.…”

Section: Discussionmentioning

confidence: 99%

“…NF-B activation is increased in colonic biopsies from IBD patients (Rogler et al, 1998;Schreiber et al, 1998), macrophages and epithelial cells isolated from inflamed IBD tissue have high levels of p65 (Rogler et al, 1998), and the level of activated NF-B correlates with the severity of disease (Rogler et al, 1998). In epithelial cells, NF-B not only contributes to the pathogenesis of IBD by altering intestinal barrier function but also activates proinflammatory signaling, potentiating the production of other proinflammatory cytokines by epithelial cells and promoting the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

Prohibitin Inhibits Tumor Necrosis Factor alpha–induced Nuclear Factor-kappa B Nuclear Translocation via the Novel Mechanism of Decreasing Importin α3 Expression

Theiss

Jenkins

Okoro

et al. 2009

MBoC

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Nuclear factor κB is activated in macrophages and epithelial cells of inflamed intestinal mucosa

Cited by 669 publications

References 41 publications

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

NF-kappaB, p38 MAPK and JNK are highly expressed and active in the stroma of human colonic adenomatous polyps

Prohibitin Inhibits Tumor Necrosis Factor alpha–induced Nuclear Factor-kappa B Nuclear Translocation via the Novel Mechanism of Decreasing Importin α3 Expression

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