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Title: Changes in H3K27ac following lipopolysaccharide stimulation of nasopharyngeal epithelial cells
Authors: Borghini, L
Hibberd, M 
Davila, S 
Keywords: bacterium lipopolysaccharide
histone H3
immunoglobulin enhancer binding protein
tumor necrosis factor
RELA protein, human
transcription factor RelA
tumor necrosis factor
brain region
cell stimulation
controlled study
correlation analysis
enhancer region
epithelium cell
gene locus
human cell
immune response
innate immunity
promoter region
protein binding
protein expression
drug effect
epithelium cell
gene expression regulation
tumor cell line
Cell Line, Tumor
Epithelial Cells
Gene Expression Regulation
Immunity, Innate
Transcription Factor RelA
Tumor Necrosis Factor-alpha
Issue Date: 2018
Citation: Borghini, L, Hibberd, M, Davila, S (2018). Changes in H3K27ac following lipopolysaccharide stimulation of nasopharyngeal epithelial cells. BMC Genomics 19 (1) : 969. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Background: The epithelium is the first line of defense against pathogens. Notably the epithelial cells lining the respiratory track are crucial in sensing airborne microbes and mounting an effective immune response via the expression of target genes such as cytokines and chemokines. Gene expression regulation following microbial recognition is partly regulated by chromatin re-organization and has been described in immune cells but data from epithelial cells is not as detailed. Here, we report genome-wide changes of the H3K27ac mark, characteristic of activated enhancers and promoters, after stimulation of nasopharyngeal epithelial cells with the bacterial endotoxin Lipopolysaccharide (LPS). Results: In this study, we have identified 626 regions where the H3K27ac mark showed reproducible increase following LPS induction in epithelial cells. This indicated that sensing of LPS led to opening of the chromatin in our system. Moreover, this phenomenon seemed to happen extensively at enhancers regions and we could observe instances of Super-enhancer formation. As expected, LPS-increased H3K27ac regions were found in the vicinity of genes relevant for LPS response and these changes correlated with up-regulation of their expression. In addition, we found the induction of H3K27ac mark to overlap with the binding of one of the NF-kB members and key regulator of the innate immune response, RELA, following LPS sensing. Indeed, inhibiting the NF-kB pathway abolished the deposition of H3K27ac at the TNF locus, a target of RELA, suggesting that these two phenomena are associated. Conclusions: Enhancers' selection and activation following microbial or inflammatory stimuli has been described previously and shown to be mediated via the NF-kB pathway. Here, we demonstrate that this is also likely to occur in the case of LPS-sensing by nasopharyngeal epithelial cells as well. In addition to validating previous findings, we generated a valuable data set relevant to the host immune response to epithelial cell colonizing or infecting pathogens. © 2018 The Author(s).
Source Title: BMC Genomics
ISSN: 14712164
DOI: 10.1186/s12864-018-5295-4
Rights: Attribution 4.0 International
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