Pretreatment of LPS inhibits IFN-β-induced STAT1 phosphorylation through SOCS3 induced by LPS.

  title={Pretreatment of LPS inhibits IFN-$\beta$-induced STAT1 phosphorylation through SOCS3 induced by LPS.},
  author={Takashi Ando and Takayuki Komatsu and Yoshikazu Naiki and Takashi. Yokochi and Daisuke Watanabe and Naoki Koide},
  journal={Biomedicine \& pharmacotherapy = Biomedecine \& pharmacotherapie},
  • T. Ando, T. Komatsu, +3 authors N. Koide
  • Published 1 December 2015
  • Chemistry, Medicine
  • Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
It has been known that LPS activates macrophages and induces IFN-β production from macrophages. The endogenous IFN-β produced by LPS stimulates the cells, which plays a role in innate immune. However, it was not elucidated yet if the signaling by exogenous IFN-β was influenced by LPS stimulation. In this study, it was found pretreatment of LPS interrupted IFN-β-induced JAK1/STAT1 phosphorylation. LPS pretreatment also reduced IFN-β-induced ISG54, one of IFN-β-inducible genes. Pretreatment with… Expand

Figures and Topics from this paper

MicroRNA‐136 promotes lipopolysaccharide‐induced ATDC5 cell injury and inflammatory cytokine expression by targeting myeloid cell leukemia 1
It is verified that miR‐136 promoted LPS‐induced ATDC5 cell injury and inflammatory cytokine expression by targeting M cl‐1, and Mcl‐1 was involved in the regulatory effects of LPS on Wnt/β‐catenin and JAK/STAT signaling pathways in ATDC 5 cells. Expand
Cooking oil fume-derived PM2.5 induces apoptosis in A549 cells and MAPK/NF-кB/STAT1 pathway activation
This study suggested that COF-PM2.5 resulted in inflammation, apoptosis, and cell damage in A549 cells, which might be modulated via the activation of MAPK/NF-кB/STAT1 pathway. Expand
The impact of plasma SOCS3 levels and endometrial leukocytes on unexplained infertility
The interaction between plasma SOCS3 levels and staining degree of endometrial leukocytes may be either the reason for or result of infertility leading to unavailability of the environment for implantation. Expand


Lipopolysaccharide induces in macrophages the synthesis of the suppressor of cytokine signaling 3 and suppresses signal transduction in response to the activating factor IFN-gamma.
The results link the deactivating effect of chronic LPS exposure on macrophages with its ability to induce SOCS3 with the LPS-dependent reduction of IFN-gamma-mediated Janus kinase 1 (JAK1) activation. Expand
Lipopolysaccharide-induced Expression of Interferon-β Mediates the Timing of Inducible Nitric-oxide Synthase Induction in RAW 264.7 Macrophages*
It is proposed that the cytokine environment of macrophages may determine the rate and magnitude of nitric oxide production, thereby regulating the cytotoxic response to pathogen challenge. Expand
Bacterial lipopolysaccharide and gamma interferon induce transcription of beta interferon mRNA and interferon secretion in murine macrophages
The induction ofIFN-beta by IFN-gamma appears to be a characteristic response of PM and may be at least in part responsible for the resistance of these cells to viral infections. Expand
IL-10 Inhibits Lipopolysaccharide-Induced CD40 Gene Expression through Induction of Suppressor of Cytokine Signaling-3
IL-10 and LPS synergize to induce suppressor of cytokine signaling (SOCS)-3 gene expression in macrophages and microglia, and results indicate that SOCS-3 plays an important role in the negative regulation of LPS-induced CD40 gene expression by IL-10. Expand
Role of interferons in LPS hypersensitivity
It is shown that Gram-negative bacteria induce IFN-γ in mice also by an IFN -β-dependent pathway that requires IL-18 and is independent of IL-12 signaling, the activation of which is directly linked toIFN-β. Expand
Low responsiveness to IFN‐γ, after pretreatment of mouse macrophages with lipopolysaccharides, develops via diverse regulatory pathways
We have investigated the mechanisms by which prior exposure of mouse macrophages to lipopolysaccharides (LPS) induces a state of low responsiveness to subsequent exposure to IFN‐γ. We demonstrateExpand
LPS and TNFα induce SOCS3 mRNA and inhibit IL‐6‐induced activation of STAT3 in macrophages
It is shown that LPS and TNFα are potent inhibitors of IL‐6‐mediated STAT3 activation in human monocyte derived macrophages, rat liver Macrophages and RAW 264.7 mouse macrophage but not in human hepatoma cells (HepG2) or in rat hepatocytes. Expand
Indirect induction of suppressor of cytokine signalling-1 in macrophages stimulated with bacterial lipopolysaccharide: partial role of autocrine/paracrine interferon-alpha/beta.
It is shown that mouse IFN-beta directly induces the synthesis of SOCS-1, without the need for prior protein synthesis, and does so with faster kinetics than does LPS, consistent with the non-specific nature of LPS-induced tolerance. Expand
Molecular Mechanism of Lipopolysaccharide-Induced SOCS-3 Gene Expression in Macrophages and Microglia1
Results indicate that LPS-induced MAPK activation, the production of endogenous IL-10, and STAT-3 activation play critical roles in SOCS-3 expression, which provides for feedback attenuation of cytokine-induced immune and inflammatory responses in macrophages and microglia. Expand
IFN‐β‐induced SOCS‐1 negatively regulates CD40 gene expression in macrophages and microglia
  • H. Qin, Cynthia A. Wilson, S. J. Lee, E. Benveniste
  • Biology, Medicine
  • FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2006
The molecular basis by which IFN‐β, a cytokine with immunomodulatory properties, regulates CD40 gene expression is described, and novel results indicate that IFN-β‐induced SOCS‐1 plays an important role in the negative regulation of IFn‐β‐ induced CD40Gene expression. Expand