Dexamethasone inhibits IL-1β gene expression in LPS-stimulated RAW 264.7 cells by blocking NF-κB/Rel and AP-1 activation

Jeon, Young Jin; Han, Seung Hyun; Lee, Yong W; Lee, Michael; Yang, Kyu Hwan; Kim, Hwan Mook

doi:10.1016/s0162-3109(00)00199-5

Cited by 100 publications

(70 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These include IL-1␣, IL-1␤, IL-8, interferon-␣/␤ Ra, MIP-1␣, interferon (INF)-␣/␤ Rb, IL-2, IL-6 receptor, IL-1 receptor, IL-5 receptor, IL-10, IL-10 receptor-␣, TNF-␣, INF-␥, IL-7, IL-2 receptor ␤, and IL-7 receptor. 9 Furthermore, hints at mechanism of action may be provided by noting that many of the up-regulated genes are under the transcriptional activation control of nuclear factor-B (NF-B) promoters such as IL-1␤, 18 osteoprotogerin, and perhaps osteopontin, 19 IL-8, 20 and MMP-9. 21 On this basis, it is possible that prostratin can function through the zeta isoform of PKC (PKC-), which activates NF-B.…”

Section: Discussionmentioning

confidence: 99%

Prostratin: activation of latent HIV-1 expression suggests a potential inductive adjuvant therapy for HAART

Kulkosky

Culnan

Roman

et al. 2001

Blood

299

301

View full text Add to dashboard Cite

Prostratin is a unique phorbol ester that stimulates protein kinase C activity but is nontumor promoting. Remarkably, prostratin is also able to inhibit de novo human immunodeficiency virus type 1 (HIV-1) infection yet up-regulate viral expression from latent proviruses. Prostratin's lack of tumor promotion, coupled with its ability to block viral spread yet induce latent proviral expression, prompted studies to determine whether this compound could serve as an inductive adjuvant therapy for patients treated with highly active antiretroviral therapy (HAART).

show abstract

Section: Discussionmentioning

confidence: 99%

Prostratin: activation of latent HIV-1 expression suggests a potential inductive adjuvant therapy for HAART

Kulkosky

Culnan

Roman

et al. 2001

Blood

299

301

View full text Add to dashboard Cite

show abstract

“…Glucocorticoids reduce airway hyperreactivity in the asthmatic airways [36][37][38][39] and diminish airway inflammation via inhibition of the transcription factors AP-1 and NF-kB activities [28,29,[33][34][35]. Dexamethasone inhibits the inducible bradykinin receptor expression in cultured human airway fibroblasts and smooth muscle cells [15,16].…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids suppress transcriptional up‐regulation of bradykinin receptors in a murine in vitro model of chronic airway inflammation

Zhang

Adner

Cardell

2005

Clin Experimental Allergy

View full text Add to dashboard Cite

show abstract

“…Inflammatory stimuli such as lipopolysaccharide (LPS) and IL-1b itself have been shown to activate the IL-1b gene mainly via NF-jB and AP-1 elements, depending on the cell type (Fenton 1992;Hiscott et al 1993;Sang et al 1999;Jeon et al 2000). In addition, there is an LPS-responsive 3¢-UTR element in the IL-1b mRNA sequence that is involved in the stabilization of the IL-1b mRNA (Kern et al 1997).…”

mentioning

confidence: 99%

The neuroprotective agents chlomethiazole and SB203580 inhibit IL‐1β signalling but not its biosynthesis in rat cortical glial cells

Simi

Porsmyr-Palmertz

Hjertén

et al. 2002

Journal of Neurochemistry

View full text Add to dashboard Cite

Chlomethiazole and pyridinyl imidazole compounds, exemplified by SB203580, are structurally distinct p38 mitogenactivated protein kinase inhibitors with neuroprotective properties in models of cerebral ischaemia. We have examined their effects in interleukin-1b (IL-1b) synthesis, release and signalling in rat cortical glial cells, given the important role of IL-1b in cerebral ischaemia. We analysed (i) IL-1b mRNA expression by northern blot, (ii) IL-1b protein precursor levels within the cells by western blot, and (iii) the levels of the mature IL-1b protein secreted into the medium by enzymelinked immunosorbent assay (ELISA) after treatment of rat cortical glial cells with lipopolysaccharide. While the induction of IL-1b expression by lipopolysaccharide or by IL-1b itself was very sensitive to nuclear factor kappa B (NF-jB) inhibitors, chlomethiazole or SB203580 were nearly without effect, indicating a differential regulation as compared to peripheral cells, e.g. monocytes. In contrast, chlomethiazole and SB203580 potently inhibited the IL-1b-induced expression of c-fos and inducible nitric oxide synthase, as monitored by northern blot and quantitative RT-PCR, respectively. Because IL-1b-induced expression of c-fos and inducible nitric oxide synthase is believed to directly contribute to the pathology of cerebral ischaemic injury, the results suggest a direct mechanism for the neuroprotective effects of chlomethiazole and SB203580, and further establish the anti-inflammatory properties of chlomethiazole. Keywords: chlomethiazole, glia, interleukin-1b, neuroprotection, p38 MAP kinase. Interleukin-1b (IL-1b) is a pro-inflammatory cytokine which is released by a variety of cell types, including peripheral immune cells as well as cells of the CNS-like astrocytes, microglia and some neurones (Dinarello 1988;Hopkins and Rothwell 1995). It serves a broad array of functions both in the periphery and in the CNS, and is involved in the immune-to-brain communication initiating the so-called Ôsickness responseÕ, such as the induction of fever in response to an invasion by a pathogen (for review see Rothwell 1997).Within the CNS, IL-1b is increased in response to brain injury and subsequently regulates the brain's inflammatory response by stimulating the production of other cytokines, such as IL-6 and IL-8, as well as inducible nitric oxide synthase (iNOS), chemotactic factors and adhesion molecules, for attracting peripheral mononuclear cells to cross the blood-brain barrier (Benveniste et al. 1990;Yamasaki et al. 1995;. In cases such as cerebral ischaemia and excitotoxic brain injury, IL-1b levels dramatically increase in the brain within few hours (Minami et al. 1991;Woodroofe et al. 1991;Taupin et al. 1993), and several studies have shown that inhibition or gene disruption of the Received March 12, 2002; revised manuscript received July 18, 2002; accepted August 19, 2002. Address correspondence and reprint requests to Anastasia Simi, Institute for Environmental Medicine, Division of Molecular Toxicology, Karo...

show abstract

Dexamethasone inhibits IL-1β gene expression in LPS-stimulated RAW 264.7 cells by blocking NF-κB/Rel and AP-1 activation

Cited by 100 publications

References 39 publications

Prostratin: activation of latent HIV-1 expression suggests a potential inductive adjuvant therapy for HAART

Prostratin: activation of latent HIV-1 expression suggests a potential inductive adjuvant therapy for HAART

Glucocorticoids suppress transcriptional up‐regulation of bradykinin receptors in a murine in vitro model of chronic airway inflammation

The neuroprotective agents chlomethiazole and SB203580 inhibit IL‐1β signalling but not its biosynthesis in rat cortical glial cells

Contact Info

Product

Resources

About