Tissue-Specific Differential Expression of Novel Genes and Long Intergenic Noncoding RNAs in Humans With Extreme Response to Evoked Endotoxemia

Circ Genom Precis Med. 2018 Nov;11(11):e001907. doi: 10.1161/CIRCGEN.117.001907.

Abstract

Background: Cytokine responses to activation of innate immunity differ between individuals, yet the genomic and tissue-specific transcriptomic determinants of inflammatory responsiveness are not well understood. We hypothesized that tissue-specific mRNA and long intergenic noncoding RNA (lincRNA) induction differs between individuals with divergent evoked inflammatory responses.

Methods: In the GENE Study (Genetics of Evoked Response to Niacin and Endotoxemia), we performed an inpatient endotoxin challenge (1 ng/kg lipopolysaccharide [LPS]) in healthy humans. We selected individuals in the top (high responders) and bottom (low responders) extremes of inflammatory responses and applied RNA sequencing to CD14 monocytes (N=15) and adipose tissue (N=25) before and after LPS administration.

Results: Although only a small number of genes were differentially expressed at baseline, there were clear differences in the magnitude of the transcriptional response post-LPS between high and low responders, with a far greater number of genes differentially expressed by endotoxemia in high responders. Furthermore, tissue responses differed during inflammation, and we found a number of tissue-specific differentially expressed lincRNAs post-LPS, which we validated. Relative to nondifferentially expressed lincRNAs, differentially expressed lincRNAs were equally likely to be nonconserved as conserved between human and mouse, indicating that conservation is not a predictor of lincRNAs associated with human inflammatory pathophysiology. Differentially expressed genes also were enriched for signals with inflammatory and cardiometabolic disease in published genome-wide association studies. CTB-41I6.2 ( AC002091.1), a nonconserved human-specific lincRNA, is one of the top lincRNAs regulated by endotoxemia in monocytes, but not in adipose tissue. Knockdown experiments in THP-1 monocytes suggest that this lincRNA enhances LPS-induced interleukin 6 ( IL6) expression in monocytes, and we now refer to this as monocyte LPS-induced lincRNA regulator of IL6 ( MOLRIL6).

Conclusions: We highlight mRNAs and lincRNAs that represent novel candidates for modulation of innate immune and metabolic responses in humans.

Clinical trial registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT00953667.

Keywords: adipose tissue; endotoxemia; inflammation; monocyte; response syndrome; systemic inflammatory.

Publication types

  • Clinical Trial
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / immunology*
  • Adipose Tissue / pathology
  • Animals
  • Endotoxemia* / genetics
  • Endotoxemia* / immunology
  • Endotoxemia* / pathology
  • Female
  • Gene Expression Regulation / immunology*
  • Genome-Wide Association Study
  • Humans
  • Immunity, Innate / genetics
  • Inflammation / genetics
  • Inflammation / immunology
  • Male
  • Mice
  • Monocytes / immunology*
  • Monocytes / pathology
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / immunology
  • RNA, Messenger* / genetics
  • RNA, Messenger* / immunology
  • Sequence Analysis, RNA

Substances

  • RNA, Long Noncoding
  • RNA, Messenger

Associated data

  • ClinicalTrials.gov/NCT00953667