Induction of nitric oxid synthase(NOS) by soluble glucocorticoid induced tumor necrosis factor receptor(sGITR) is modulated by IFN-γ in murine macrophage

Shin, Hong Ju; Lee, Hyeon Woo; Choi, Hye‐Seon

doi:10.1038/emm.2003.24

Cited by 18 publications

(9 citation statements)

References 2 publications

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“…Because macrophages express both GITR and GITRL, the increased expression of GITR may both positively modulate GITR-mediated pathways and trigger GITRL. In fact, recent studies demonstrate that GITRL can activate cytoplasmic signals following GITR binding (8,13,14,16,42). Future studies will clarify whether these mechanisms are both crucial in determining the decreased response of GITR Ϫ/Ϫ mice to carrageenan treatment.…”

Section: Discussionmentioning

confidence: 95%

Proinflammatory Role of Glucocorticoid-Induced TNF Receptor-Related Gene in Acute Lung Inflammation

Cuzzocrea

Nocentini

Paola

et al. 2006

The Journal of Immunology

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Glucocorticoid-induced TNFR-related gene (GITR) participates in the immune/inflammatory response. Because GITR expression has been described in cells other than T lymphocytes, we investigated whether it also modulates acute inflammatory response. Using GITR-deficient (GITR−/−) mice, we analyzed the role of GITR in the development of carrageenan-induced lung inflammation (pleurisy) by studying several proinflammatory markers 2–8 h after carrageenan injection. When compared with GITR+/+, GITR−/− mice exhibited decreased production of turbid exudate containing a lower number of leukocytes. This was correlated with the reduction of inflammatory markers (including TNF-α, IL-1β, myeloperoxidase, inducible NO synthase, and cyclooxygenase 2) in the pleural exudate and/or in the lung. Moreover, endothelial cells expressed lower levels of adhesion molecules. In lungs of GITR+/+ mice, GITR ligand expression was not modulated during pleurisy, while that of GITR increased, as a consequence of increased infiltration by GITR-expressing cells and of GITR up-regulation in macrophages and endothelial cells. Finally, cotreatment of GITR+/+ mice with carrageenan and Fc-GITR fusion protein decreased the number of inflammatory cells (pleural macrophages and lung neutrophils) as compared with carrageenan treatment alone, confirming that GITR plays a role in the modulation of pleurisy.

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Section: Discussionmentioning

confidence: 95%

Proinflammatory Role of Glucocorticoid-Induced TNF Receptor-Related Gene in Acute Lung Inflammation

Cuzzocrea

Nocentini

Paola

et al. 2006

The Journal of Immunology

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“…In fact, evidence in other experimental models suggests that GITRL can activate cytoplasmic signals in a number of cells, including dendritic cells, where GITRL triggering by GITR inhibits IL-12 production and increases tryptophan catabolism, thus favoring a tolerogenic phenotype that could account for a decreased inflammation Grohmann et al, 2007). Moreover, results in other studies indicate that GITRL triggering on APC promotes inflammatory response (Shin et al, 2003;Kim et al, 2006). In the present experimental model we show that a milder inflammatory response was induced in GITR Ϫ/Ϫ compared with GITR ϩ/ϩ mice, but also that GITR-Fc administration exerted no significative effect in SCI-GITR Ϫ/Ϫ mice but was effective in SCI-GITR ϩ/ϩ .…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid-Induced Tumor Necrosis Factor Receptor-Related (GITR)-Fc Fusion Protein Inhibits GITR Triggering and Protects from the Inflammatory Response after Spinal Cord Injury

Nocentini

Cuzzocrea

Genovese³

et al. 2008

Mol Pharmacol

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“…Chaisson et al (2002) have shown that TNF-α activates NF-κB in many cells after intraperitoneal injection. Inducible nitric oxide synthase (iNOS) transcription is also induced by TNF-α and IL-6 through NF-κB activity (Shin et al, 2003); this occurs mainly in hepatocytes just after partial hepatectomy and before cell proliferation (Loughran et al, 2005). The most important growth factor involved in hepatocyte proliferation, HGF, signals through its receptor c-Met, a transmembrane tyrosine kinase protein product of the proto-oncogene with the same name (Huh et al, 2004).…”

Section: Nf-kb Promotes Liver Regenerationmentioning

confidence: 99%

NF‐κB in liver diseases: a target for drug therapy

Muriel

2008

J of Applied Toxicology

148

106

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There are five nuclear factor-kB (NF-kB) transcription factors with important roles in innate immunity, liver inflammation, fibrosis and apoptosis prevention. Several inhibitors of NF-kB, like caffeic acid, captopril, curcumin, pyrrolidine dithiocarbamate, resveratrol, silymarin and thalidomide, have demonstrated antinecrotic, anticholestatic, antifibrotic and anticancer activities in the liver. A link between inflammation and hepatocellular carcinoma through the NF-kB pathway has been observed, providing ample experimental support for the tumor-promoting function of NF-kB in various models of cancer. NF-kB has been associated with the induction of proinflammatory gene expression and has attracted interest as a target for the treatment of inflammatory disease. However, despite much attention being focused on the deleterious effects of NF-kB, activation of this factor during the resolution of inflammation is associated with the production of antiinflammatory molecules like interleukin (IL)-10 and the onset of apoptosis. This suggests that NF-kB has an antiinflammatory role in vivo involving the regulation of the resolution of inflammation. Also, NF-kB promotes liver regeneration by upregulating IL-6 and other molecules like hepatocyte growth factor. It has been postulated that the beneficial properties of NF-kB are due to p50 homodimers, whose activation prevents cholestatic and chronic liver injury. More basic understanding on the function of the diverse NF-kB factors is urgently needed in different physiological and pathological conditions, because depending on the subunit composition of the dimmer, the disease and the stage of the illness, inhibition of the factor may result in a beneficial or in a deleterious response. Copyright © 2008 John Wiley & Sons, Ltd.There are five nuclear factor-kB (NF-kB) transcription factors with important roles in innate immunity, liver inflammation, fibrosis, and apoptosis prevention. Several inhibitors of NF-kB have demonstrated antinecrotic, anticholestatic, antifibrotic and anticancer activities in the

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Induction of nitric oxid synthase(NOS) by soluble glucocorticoid induced tumor necrosis factor receptor(sGITR) is modulated by IFN-γ in murine macrophage

Cited by 18 publications

References 2 publications

Proinflammatory Role of Glucocorticoid-Induced TNF Receptor-Related Gene in Acute Lung Inflammation

Proinflammatory Role of Glucocorticoid-Induced TNF Receptor-Related Gene in Acute Lung Inflammation

Glucocorticoid-Induced Tumor Necrosis Factor Receptor-Related (GITR)-Fc Fusion Protein Inhibits GITR Triggering and Protects from the Inflammatory Response after Spinal Cord Injury

NF‐κB in liver diseases: a target for drug therapy

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