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Fig. 4 | Journal of Inflammation

Fig. 4

From: Histone H3 posttranslational modified enzymes defined neutrophil plasticity and their vulnerability to IL-10 in the course of the inflammation

Fig. 4

Neutrophils stimulated by IL-10, LPS, or TNF-regulated gene positioning specific profile of PTMs via H3K4me3 during different states of inflammation (pre-activation, activation or suppression). A Gene Ontology analysis of the Biological processes responsible for chromatin organisation mediated methylation and demethylation within histone H3 by positioning H3K4me3 methylation. Methylation of H3K4me3 is the process that dominates regardless of whether neutrophils are exposed to pro- or anti-inflammatory factors. Pro- vs. anti-inflammatory stimuli differences are determined via H3K4me3 ‘de positioning’ methylation of histone H3K9. The green arrow points to the demethylation of H3K9 as the process triggered upon exposure to IL-10. The red one points to H3K4me3 trimethylation as the parent process of neutrophil polarisation regardless of stimuli. Data are presented as mean values calculated from four independent experiments. B Binding site overlap in the GO term ‘Chromatin Organization’, ‘Histone H3K4-trimethylation’ and ‘Histone demethylase activity H3K9 specific’; n.s, non-stimulated. The analysis of target genes in the GO terms Chromatin organisation are presented in Supplementary Table 1. C The comparison of peak density within PTM enzymes revealed high signal within TSSs (Exon 1) of MLL1 and SETD1A in neutrophils stimulated by LPS and increased density within CHD1 as well as JMJD2A in neutrophils exposed to IL-10

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