Dysregulation of JAK/STAT genes by vasoactive intestinal peptide (VIP) in Salmonella-infected monocytes may inhibit its therapeutic potential in human sepsis

Cytokine. 2018 May:105:49-56. doi: 10.1016/j.cyto.2018.02.014. Epub 2018 Feb 16.

Abstract

Murine/LPS models of Gram negative sepsis indicate that vasoactive intestinal peptide (VIP) has therapeutic potential. We investigated the unknown effect of VIP on JAK/STAT proteins and genes in human monocytes infected with Salmonella Typhimurium 14028. S. Typhimurium 14028 increased expression of both IL-6 receptor (IL-6R) and interferon gamma receptor 1 (IFNγR1) on monocytes but co-culture of infected monocytes with VIP (10-7 M) only decreased expression of IFNγR1 (P < 0.05). In contrast, S. Typhimurium 14028 infection or co-culture with VIP had no effect on IL-10 receptor expression on the monocyte surface. However, S. Typhimurium 14028 down regulated IFNGR1 gene expression and this was not altered by co-culture with VIP, suggesting that changes in IFNγR1 protein may be due to an effect on cytoplasmic transport. 15 JAK/STAT genes, out of 84 studied, were up-regulated by S. Typhimurium 14028 infection and five were down-regulated. Co-culture with VIP significantly decreased expression of two genes (IFNG and IL-20) and increased expression of three genes (SOCS1, SOCS3 and STAT4) (P < 0.05). S. Typhimurium 14028 also increased expression of PTPN1, which dephosphorylates JAK2 and TYK2. This was unaltered by co-culture with VIP but S. Typhimurium 14028-induced expression of ISG15, associated with susceptibility to Gram negative infection, was further increased by VIP. We conclude that the effect of VIP on JAK/STAT genes may preclude its therapeutic use in human Gram negative sepsis.

Keywords: IFN-γRα; JAK/STAT; Monocyte; Salmonella; VIP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Survival / drug effects
  • Cell Survival / genetics
  • Down-Regulation / drug effects
  • Down-Regulation / genetics
  • Gene Expression Regulation / drug effects*
  • Humans
  • Janus Kinases / genetics*
  • Monocytes / drug effects
  • Monocytes / microbiology*
  • Receptors, Cytokine / metabolism
  • STAT Transcription Factors / genetics*
  • Salmonella typhimurium / physiology*
  • Sepsis / genetics*
  • Sepsis / microbiology*
  • Sepsis / pathology
  • Up-Regulation / drug effects
  • Up-Regulation / genetics
  • Vasoactive Intestinal Peptide / pharmacology*

Substances

  • Receptors, Cytokine
  • STAT Transcription Factors
  • Vasoactive Intestinal Peptide
  • Janus Kinases