SULFORAPHANE EPIGENETICALLY REGULATES THE LPS-INDUCED KINETICS OF INNATE IMMUNE RESPONSE IN PORCINE MONOCYTE-DERIVED DENDRITIC CELLS

ÇINAR M. U.

The 2014 Innate Immunity Summit, London, United Kingdom, 10 - 12 November 2014, pp.1, (Summary Text)

  • Publication Type: Conference Paper / Summary Text
  • City: London
  • Country: United Kingdom
  • Page Numbers: pp.1
  • Erciyes University Affiliated: Yes

Abstract

Dendritic cell (DC) plays an essential role in detection of microbial attack in innate immune system. Activated DCs can induce acute inflammation and sepsis upon exposure to microbial if excessive signals occur. The epigenetic mechanisms involve in the development and differentiation of innate immune system, and consequently that of related pathologies (autoimmune diseases and hematological disorder), has advanced considerably in recent years. Histone acetylation is a key epigenetic modification controlling chromatin structure, DNA accessibility for transcription factor and gene expression. HDAC inhibitor sulforaphane (SFN) exhibits anti-oxidative, antimicrobial, anti-inflammatory, and anti-tumoral properties with inhibition of HDAC activity. In the present study we aimed to investigate the effects of SFN on the expression and kinetics of cytokine productions, we further analyzed the importance of SNF on the regulation of innate immune response with directly against the DCs maturation and enhancement of the phagocytosis in response to LPS stimulation through epigenetic modifications in porcine monocyte-derived dendritic cells (moDCs). The present work provides the first evidence that the SFN supplementation in vitro acts as the HDAC inhibitor in porcine moDCs with inhibition of HDAC activity. HDAC inhibitor SFN exerts profound dynamic administration on the moDCs innate immune antimicrobial against response in different pathogen challenging stages, down-regulated the expression of innate immune receptor, interfered with transcription factors remodeling and inhibited the expression of key antimicrobial cytokines and accessory molecules in the early stage after LPS stimulation. Conversely, SFN promoted the immune gene including cytokine expressions after 6 h LPS stimulation. Consistent with these dynamic immune-mediatory effects in LPS induction, we might suspect that SFN enhances the tolerance of moDCs and protects host cells from the inflammatory risk to bacterial infection.