A novel small compound SH-2251 suppresses Th2 cell-dependent airway inflammation through selective modulation of chromatin status at the Il5 gene locus

PLoS One. 2013 Apr 16;8(4):e61785. doi: 10.1371/journal.pone.0061785. Print 2013.

Abstract

IL-5 is a key cytokine that plays an important role in the development of pathological conditions in allergic inflammation. Identifying strategies to inhibit IL-5 production is important in order to establish new therapies for treating allergic inflammation. We found that SH-2251, a novel thioamide-related small compound, selectively inhibits the differentiation of IL-5-producing Th2 cells. SH-2251 inhibited the induction of active histone marks at the Il5 gene locus during Th2 cell differentiation. The recruitment of RNA polymerase II, and following expression of the Th2 cell-specific intergenic transcripts around the Il5 gene locus was also inhibited. Furthermore, Th2 cell-dependent airway inflammation in mice was suppressed by the oral administration of SH-2251. Gfi1, a transcriptional repressor, was identified as a downstream target molecule of SH-2251 using a DNA microarray analysis. The Gfi1 expression dramatically decreased in SH-2251-treated Th2 cells, and the SH-2251-mediated inhibition of IL-5-producing Th2 cell differentiation was restored by transduction of Gfi1. Therefore, our study unearthed SH-2251 as a novel therapeutic candidate for allergic inflammation that selectively inhibits active histone marks at the Il5 gene locus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use*
  • CD4-Positive T-Lymphocytes / metabolism
  • Chromatin / drug effects
  • Chromatin / metabolism*
  • Chromatin Immunoprecipitation
  • Enzyme-Linked Immunosorbent Assay
  • Immunoblotting
  • Inflammation / drug therapy*
  • Interleukin-5 / genetics*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Oligonucleotide Array Sequence Analysis / methods
  • Respiratory Hypersensitivity / drug therapy
  • Reverse Transcriptase Polymerase Chain Reaction
  • Th2 Cells / metabolism*

Substances

  • Anti-Inflammatory Agents
  • Chromatin
  • Interleukin-5

Grants and funding

This work was supported by the Global COE Program (Global Center for Education and Research in Immune System Regulation and Treatment), JST PRESTO (Japan), and by grants from the Ministry of Education, Culture, Sports, Science and Technology (Japan) (Grants-in-Aid: Scientific Research (B) #23390075). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.