TNFα- and NF-κB-dependent induction of the chemokine CCL1 in human macrophages exposed to the atherogenic lipoprotein(a)

N’Diaye, Monique; Ferrec, Eric Le; Kronenberg, Florian; Dieplinger, Hans; Vée, Marc Le; Fardel, Olivier

doi:10.1016/j.lfs.2009.01.012

Cited by 12 publications

(5 citation statements)

References 45 publications

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“…Indeed, infliximab abolished CCL1 gene expression and protein secretion (Figure 4E, F, respectively) in tolerant iDCs indicating that TNF-α plays a major role in PGN-induced CCL1 expression. This is in agreement with the finding showing that TNF-α induces the expression of CCL1 in macrophages [43]. Taking into account recent reports demonstrating elevated CCL1 expression is atopic dermatitis [42,44] our results may provide an additional explanation for the successful application of anti-TNF-α therapy in atopic dermatitis [40]: by targeting TNF-α the downstream expression of CCL1 is decreased attenuating thereby the initiation and amplification of atopic skin inflammation.…”

Section: Resultssupporting

confidence: 92%

Genome Wide Transcriptome Analysis of Dendritic Cells Identifies Genes with Altered Expression in Psoriasis

et al. 2013

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Activation of dendritic cells by different pathogens induces the secretion of proinflammatory mediators resulting in local inflammation. Importantly, innate immunity must be properly controlled, as its continuous activation leads to the development of chronic inflammatory diseases such as psoriasis. Lipopolysaccharide (LPS) or peptidoglycan (PGN) induced tolerance, a phenomenon of transient unresponsiveness of cells to repeated or prolonged stimulation, proved valuable model for the study of chronic inflammation. Thus, the aim of this study was the identification of the transcriptional diversity of primary human immature dendritic cells (iDCs) upon PGN induced tolerance. Using SAGE-Seq approach, a tag-based transcriptome sequencing method, we investigated gene expression changes of primary human iDCs upon stimulation or restimulation with Staphylococcus aureus derived PGN, a widely used TLR2 ligand. Based on the expression pattern of the altered genes, we identified non-tolerizeable and tolerizeable genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (Kegg) analysis showed marked enrichment of immune-, cell cycle- and apoptosis related genes. In parallel to the marked induction of proinflammatory mediators, negative feedback regulators of innate immunity, such as TNFAIP3, TNFAIP8, Tyro3 and Mer are markedly downregulated in tolerant cells. We also demonstrate, that the expression pattern of TNFAIP3 and TNFAIP8 is altered in both lesional, and non-lesional skin of psoriatic patients. Finally, we show that pretreatment of immature dendritic cells with anti-TNF-α inhibits the expression of IL-6 and CCL1 in tolerant iDCs and partially releases the suppression of TNFAIP8. Our findings suggest that after PGN stimulation/restimulation the host cell utilizes different mechanisms in order to maintain critical balance between inflammation and tolerance. Importantly, the transcriptome sequencing of stimulated/restimulated iDCs identified numerous genes with altered expression to date not associated with role in chronic inflammation, underlying the relevance of our in vitro model for further characterization of IFN-primed iDCs.

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Section: Resultssupporting

confidence: 92%

Genome Wide Transcriptome Analysis of Dendritic Cells Identifies Genes with Altered Expression in Psoriasis

et al. 2013

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“…Interestingly, it has also been shown that NF-B activation accompanies Lp(a) stimulation of CCL1 expression in macrophages ( 41 ). On this basis, we hypothesized a role for NF-B and AP-1 in the enhancement of IL-8 expression in THP-1 cells downstream of MAPK signaling pathway activation in response to apo(a) treatment.…”

Section: Discussionmentioning

confidence: 79%

Mechanistic insights into Lp(a)-induced IL-8 expression: a role for oxidized phospholipid modification of apo(a)

Scipione

Sayegh

Romagnuolo

et al. 2015

Journal of Lipid Research

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“…DNA binding of p65 NF‐κB was analyzed using the ELISA‐based TransAM NF‐κB kit (Active Motif, Rixensart, Belgium) as previously described .…”

Section: Methodsmentioning

confidence: 99%

The aryl hydrocarbon receptor is functionally upregulated early in the course of human T‐cell activation

et al. 2014

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TNFα- and NF-κB-dependent induction of the chemokine CCL1 in human macrophages exposed to the atherogenic lipoprotein(a)

Cited by 12 publications

References 45 publications

Genome Wide Transcriptome Analysis of Dendritic Cells Identifies Genes with Altered Expression in Psoriasis

Genome Wide Transcriptome Analysis of Dendritic Cells Identifies Genes with Altered Expression in Psoriasis

Mechanistic insights into Lp(a)-induced IL-8 expression: a role for oxidized phospholipid modification of apo(a)

The aryl hydrocarbon receptor is functionally upregulated early in the course of human T‐cell activation

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