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Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

ABSTRACT: Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

PROVIDER: PRJEB5869 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR458836_1.fastq.gz	Fastqsanger.gz
	ERR458836_2.fastq.gz	Fastqsanger.gz
	ERR458837_1.fastq.gz	Fastqsanger.gz
	ERR458837_2.fastq.gz	Fastqsanger.gz
	ERR458838_1.fastq.gz	Fastqsanger.gz

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Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

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Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes - microarray study

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Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes.

Project description:Early reports indicate that long non-coding RNAs (lncRNAs) are novel regulators of biological responses. However, their role in the human innate immune response, which provides the initial defence against infection, is largely unexplored. To address this issue, here we characterize the long non-coding RNA transcriptome in primary human monocytes using RNA sequencing. We identify 76 enhancer RNAs (eRNAs), 40 canonical lncRNAs, 65 antisense lncRNAs and 35 regions of bidirectional transcription (RBT) that are differentially expressed in response to bacterial lipopolysaccharide (LPS). Crucially, we demonstrate that knockdown of nuclear-localized, NF-κB-regulated, eRNAs (IL1β-eRNA) and RBT (IL1β-RBT46) surrounding the IL1β locus, attenuates LPS-induced messenger RNA transcription and release of the proinflammatory mediators, IL1β and CXCL8. We predict that lncRNAs can be important regulators of the human innate immune response.

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Bacterial non-coding RNAs excised from within protein-coding transcripts

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Project description:This study examines patterns of genome-wide transcriptional response to the active form of vitamin D, 1,25-dihyroxyvitamin D3 (1,25D), and the bacterial lipopolysaccharide (LPS) in primary human monocytes, to better understand pathways underlying the immunomodulatory role of 1,25D. Total RNA extraced from monocytes from 20 healthy individuals of African-African and European-American ancestry treated with 1,25D alone or in the presence of LPS for 24 hours.

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Project description:Monocytes are key players in innate immunity, with their ability to regulate inflammatory responses and combat invading pathogens. There is a growing body of evidence indicating that long non-coding RNA (lncRNA) participate in various cellular biological processes, including the innate immune response. The immunoregulatory properties of numerous lncRNAs discovered in monocytes remain largely unexplored. In this study, we used RNA sequencing data of circulatory blood monocytes obtained from sepsis patients to identify the elevated antisense lncRNA JHMD1D-AS1, relative to healthy participants. We subsequently demonstrated that in both circulatory blood monocytes and monocyte-derived macrophages exposed to TLR-agonists, JHMD1D-AS1 expression was induced in a temporal specific manner. Using small interfering RNA (siRNA) electroporation to render monocytes deficient of JHDM1D-AS1 and over-expression experiments, we revealed a role for lncRNA JHDM1D-AS1 in cell development, as well as in restraining pro-inflammatory gene expression. Altogether, these findings identify antisense lncRNA JHDM1D-AS1 as a potential repressor of the inflammatory response in human primary monocytes and macrophages.

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