Increased production of luminol enhanced chemiluminescence by the inflamed colonic mucosa in patients with ulcerative colitis.

Sedghi, Shahriar; Fields, Jeremy Z.; Klamut, M; Urban, G; Durkin, Margaret M.; Winship, Daniel H.; Fretland, D. J.; Olyaee, Mojtaba; Keshavarzian, Ali

doi:10.1136/gut.34.9.1191

Cited by 94 publications

(42 citation statements)

References 33 publications

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“…ROS-mediated cell damage is implicated in the pathogenesis of a variety of diseases (7). In the gastrointestinal tract, ROSinduced injury endothelial dysfunction is considered to be an important cellular mechanism in indomethacin-induced gastric mucosal injury (8) as well as in the colonic inflammation associated with ulcerative colitis (9). The exact cellular signaling involved in ROS-mediated intestinal cell injury in NEC is not well defined.…”

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confidence: 99%

Signal Transduction Pathways Involved in Oxidative Stress-Induced Intestinal Epithelial Cell Apoptosis

et al. 2005

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confidence: 99%

Signal Transduction Pathways Involved in Oxidative Stress-Induced Intestinal Epithelial Cell Apoptosis

et al. 2005

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“…Production of ROS from several sources initiate a cytotoxic cascade of events that culminate in cell death. Thus, stimulated inflammatory cells present in the inflamed mucosa are capable of producing superoxide anion and hydrogen peroxide (Harris et al, 1992;McKenzie et al, 1996;Simmonds and Rampton, 1993).The xantine oxidase pathway and the oxidation of arachidonic acid in colonocytes constitute additional sources of ROS (Biemond et al, 1988;Markowitz et al, 1988;Sedghi et al, 1993). The interaction of these species with specific vascular or interstitial components yield potent chemoattractants for inflammatory phagocytes, establishing a self-amplifying cycle of ROS production that may overwhelm defense strategies resulting in tissue damage (Lewis et al, 1988;Shingu and Nobunaga 1984;Zimmerman et al, 1990).…”

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confidence: 99%

Replenishment of Glutathione Levels Improves Mucosal Function in Experimental Acute Colitis

Ardite

Sans

Panés

et al. 2000

Laboratory Investigation

106

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SUMMARY:Because reactive oxygen species (ROS) have been implicated as mediators of inflammatory bowel disease (IBD), the purpose of the present work was to determine the functional role of mucosal GSH in the trinitrobenzenesulfonic acid in 50% ethanol (TNBSϩethanol)-induced colitis in rats. Mucosal samples were taken to evaluate the temporal relationship between the extent of injury, the levels of glutathione (GSH) during acute colitis induced by TNBSϩethanol, and the effect of N-acetylcysteine (NAC) administration. In vitro assays revealed the interaction of TNBS with GSH leading to the almost instantaneous disappearance of GSH, while the reductive metabolism of TNBS by GSSG reductase generated ROS. Mucosal samples from TNBSϩethanol-treated rats indicated a direct correlation between GSH depletion and injury detected as soon as 30 minutes after TNBSϩethanol administration that persisted 24 hours post treatment. Although, short term depletion of mucosal GSH per se by diethylmaleate did not result in mucosal injury, the oral administration of NAC (40 mM) 4 hours after TNBSϩethanol treatment increased GSH stores (2-fold), decreasing the extent of mucosal injury (60 -70%) examined at 24 hours post treatment. However, an equimolar dose of dithiothreitol failed to increase GSH levels and protect mucosa from TNBSϩethanol-induced injury. Interestingly, GSH levels in TNBSϩethanol-treated rats recovered by 1-2 weeks, an effect that was accounted for by an increase of ␥-glutamylcysteine synthetase (␥-GCS) activity due to an induction of ␥-GCS-heavy subunit chain mRNA. Thus, TNBS promotes two independent mechanisms of injury, GSH depletion and ROS generation, both being required for the manifestation of mucosal injury as GSH limitation renders intestine susceptible to the TNBS-induced ROS overgeneration. Accordingly, in vivo administration of NAC attenuates the acute colitis through increased mucosal GSH levels, suggesting that GSH precursors may be of relevance in the acute relapse of IBD. (Lab Invest 2000, 80:735-744).I nflammatory bowel disease (IBD) is a chronic inflammatory disorder whose etiology is not completely understood. Several factors are recognized to contribute to its development including an overgeneration of reactive oxygen species (ROS). Production of ROS from several sources initiate a cytotoxic cascade of events that culminate in cell death. Thus, stimulated inflammatory cells present in the inflamed mucosa are capable of producing superoxide anion and hydrogen peroxide (Harris et al, 1992;McKenzie et al, 1996;Simmonds and Rampton, 1993).The xantine oxidase pathway and the oxidation of arachidonic acid in colonocytes constitute additional sources of ROS (Biemond et al, 1988;Markowitz et al, 1988;Sedghi et al, 1993). The interaction of these species with specific vascular or interstitial components yield potent chemoattractants for inflammatory phagocytes, establishing a self-amplifying cycle of ROS production that may overwhelm defense strategies resulting in tissue damage (Lewis et al, 1988;Shingu and ...

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“…In IBD patients, oxidative stress occurs as a result of recurrent and abnormal inflammation. Several studies have established a correlation between the increase in reactive oxygen species (ROS) production and disease activity in inflamed biopsies of IBD patients [104][105][106][107]. Therefore, another mechanism by which LAB could prevent inflammation is through the expression of antioxidant enzymes that can degrade ROS or at least impair their formation.…”

Section: Antioxidant Enzyme-producingmentioning

confidence: 99%

Potential Application of Probiotics in the Prevention and Treatment of Inflammatory Bowel Diseases

Carmen

LeBlanc

Miyoshi

et al. 2011

Ulcers

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Lactic acid bacteria (LAB) represent a heterogeneous group of microorganisms that are naturally present in many foods and possess a wide range of therapeutic properties. The aim of this paper is to present an overview of the current expanding knowledge of the mechanisms by which LAB and other probiotic microorganisms participate in the prevention and treatment of inflammatory bowel diseases. These include changes in the gut microbiota, stimulation of the host immune responses, and reduction of the oxidative stress due to their antioxidant properties. A brief overview of the uses of genetically engineered LAB that produce either antioxidant enzymes (such as catalase and superoxide dismutase) or anti-inflammatory cytokines (such as IL-10) will also be discussed. This paper will show that probiotics should be considered in treatment protocols of IBD since they provide many beneficial effects and can enhance the effectiveness of traditional used medicines.

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Increased production of luminol enhanced chemiluminescence by the inflamed colonic mucosa in patients with ulcerative colitis.

Cited by 94 publications

References 33 publications

Signal Transduction Pathways Involved in Oxidative Stress-Induced Intestinal Epithelial Cell Apoptosis

Signal Transduction Pathways Involved in Oxidative Stress-Induced Intestinal Epithelial Cell Apoptosis

Replenishment of Glutathione Levels Improves Mucosal Function in Experimental Acute Colitis

Potential Application of Probiotics in the Prevention and Treatment of Inflammatory Bowel Diseases

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