Signal transduction by tumor necrosis factor and gene regulation of the inflammatory cytokine interleukin-6

Berghe, Wim Vanden; Vermeulen, Linda; Wilde, Gert De; Bosscher, Karolien De; Boone, Elke; Haegeman, Guy

doi:10.1016/s0006-2952(00)00412-3

Cited by 279 publications

(196 citation statements)

References 191 publications

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“…Increased ceramide synthesis in response to excessive TNF-α is associated with an inhibition of insulin signalling [1]. TNF-α is known to be involved in the regulation of IL-6 production [12]. We did not observe any association between the circulating levels of TNF-α and ceramides.…”

Section: Discussioncontrasting

confidence: 54%

“…The sphingomyelin pathway and ceramides themselves are reported to play a role in the regulation of IL6 gene expression [11], probably through the activation of transcription factors such as the nuclear factor kappa-B (NFκB) [11,12]. Ceramides can act as inducers of proinflammatory cytokines through the Log value for serum IL-6 (pg/ml) * Fig.…”

Section: Discussionmentioning

confidence: 99%

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Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease

et al. 2009

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Aims/hypothesis Ceramides and IL-6 have a role in immune-inflammatory responses and cardiovascular diseases, and are suggested to be involved in insulin and glucose metabolism. We sought to assess the associations of circulating levels of IL-6, TNF-α and high-sensitivity C reactive protein (hsCRP), which are inflammatory markers related to insulin resistance (IR), with the plasma lipid metabolites ceramides and diacylglycerols (DAG) in patients with CHD. Methods Cross-sectional analyses were carried out on data from 33 patients with CHD. Serum levels of the inflammatory markers and plasma lipid metabolites (lipidomics approach performed by ultra-performance liquid chromatography coupled to electrospray ionisation MS) were measured at the same time point as insulin resistance (IR) (HOMA-IR index).Results Serum circulating levels of IL-6 were strongly correlated with plasma ceramide concentrations (r=0.59, p<0.001). Adjustments for serum TNF-α or hsCRP levels, smoking, BMI, age, sex or HOMA-IR did not change the results (p<0.001). After adjustments for the effect of serum inflammatory markers (TNF-α or hsCRP), HOMA-IR and BMI the correlation between plasma DAG and serum IL-6 (r=0.33) was also significant (p<0.03). In a linear regression model, circulating levels of both ceramides and TNF-α had a significant independent influence on circulating levels of IL-6, altogether accounting for 41% of its variation (p<0.001). Conclusions/interpretation Our results strongly suggest that the link between ceramides, IR and inflammation is related to the inflammatory marker IL-6. Ceramides may contribute to the induction of inflammation involved in IR states that frequently coexist with CHD.

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Section: Discussioncontrasting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease

et al. 2009

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“…IL-6 has been shown to be involved in bleomycin-induced inflammation 28,29 and is produced by a variety of cell types, including epithelial cells and macrophages. 30,31 There is also good evidence that secretion of IL-6 is regulated through NF B 32 and NF B consensus binding sites have been identified in the promoter of the IL6 gene. 33,34 We also measured the effect of NF B decoy ODN on total and differential cell counts, as it is well documented that inflammatory cell chemokines, such as macrophage inflammatory protein-1␣ and macrophage inflammatory protein-2, which are involved in the generation of bleomycin-induced lung damage, 28,35 are regulated through NF B.…”

Section: Discussionmentioning

confidence: 99%

Cytoplasmic deposition of NFκB decoy oligonucleotides is insufficient to inhibit bleomycin-induced pulmonary inflammation

et al. 2002

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Lung inflammation leads to severe tissue destruction and ultimately organ failure in a number of diseases, including cystic fibrosis (CF). The transcription factor nuclear factor kappa B (NF B) regulates expression of many pro-inflammatory mediators. We have assessed the effect of topical administration of NF B decoys in a bleomycin model of acute lung inflammation. Using fluorescein-labelled decoy oligonucleotides (ODN) (80 g/mouse) we have shown that lipid-complexed and 'naked' ODN transfect conducting airway epithelium in a comparable manner (approximately 65% of cells). However, the ODN were detectable in the cytoplasm, but not in the nucleus of transfected cells. An increase of ODN dose to 500 g/mouse did not increase

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“…Increasing evidence shows that corticosteroids may exert an inhibitory effect on these pathways. Corticosteroids may inhibit AP-1 and NF-B via an inhibitory effect on c-Jun N-terminal kinases, which activate these transcription factors (37,38). Corticosteroids reduce the stability of mRNA for some inflammatory genes, such as cyclooxygenase-2, through an inhibitory action on another MAP kinase, p38 MAP kinase (39).…”

Section: Effects On Mitogen-activated Protein Kinasesmentioning

confidence: 99%

How Do Corticosteroids Work in Asthma?

2003

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Signal transduction by tumor necrosis factor and gene regulation of the inflammatory cytokine interleukin-6

Cited by 279 publications

References 191 publications

Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease

Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease

Cytoplasmic deposition of NFκB decoy oligonucleotides is insufficient to inhibit bleomycin-induced pulmonary inflammation

How Do Corticosteroids Work in Asthma?

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