5-Lipoxygenase inhibitors attenuate TNF-α-induced inflammation in human synovial fibroblasts

PLoS One. 2014 Sep 17;9(9):e107890. doi: 10.1371/journal.pone.0107890. eCollection 2014.

Abstract

The lipoxygenase isoform of 5-lipoxygenase (5-LOX) is reported to be overexpressed in human rheumatoid arthritis synovial tissue and involved in the progress of inflammatory arthritis. However, the detailed mechanism of how 5-lipoxygenase regulates the inflammatory response in arthritis synovial tissue is still unclear. The aim of this study was to investigate the involvement of lipoxygenase pathways in TNF-α-induced production of cytokines and chemokines. Human synovial fibroblasts from rheumatoid patients were used in this study. 5-LOX inhibitors and shRNA were used to examine the involvement of 5-LOX in TNF-α-induced cytokines and chemokines expression. The signaling pathways were examined by Western Blotting or immunofluorescence staining. The effect of 5-LOX inhibitor on TNF-α-induced chemokine expression and paw edema was also explored in vivo in C57BL/6 mice. Treatment with 5-LOX inhibitors significantly decreased TNF-α-induced pro-inflammatory mediators including interleukin-6 (IL-6) and monocyte chemo-attractant protein-1 (MCP-1) in human synovial fibroblasts. Knockdown of 5-LOX using shRNA exerted similar inhibitory effects. The abrogation of NF-κB activation was involved in the antagonizing effects of these inhibitors. Furthermore, 5-LOX inhibitor decreased TNF-α-induced up-regulation of serum MCP-1 level and paw edema in mouse model. Our results provide the evidence that the administration of 5-LOX inhibitors is able to ameliorate TNF-α-induced cytokine/chemokine release and paw edema, indicating that 5-LOX inhibitors may be developed for therapeutic treatment of inflammatory arthritis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arachidonate 5-Lipoxygenase / deficiency
  • Arachidonate 5-Lipoxygenase / genetics
  • Arachidonate 5-Lipoxygenase / metabolism*
  • Chemokine CCL2 / blood
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Edema / drug therapy
  • Edema / genetics
  • Edema / metabolism
  • Edema / pathology
  • Enzyme Activation / drug effects
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Gene Knockout Techniques
  • Humans
  • I-kappa B Kinase / metabolism
  • Inflammation / chemically induced
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Inflammation / pathology
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Leukotriene B4 / metabolism
  • Lipoxygenase Inhibitors / pharmacology*
  • Lipoxygenase Inhibitors / therapeutic use
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Phosphorylation / drug effects
  • Proteolysis / drug effects
  • RNA Interference
  • RNA, Small Interfering / genetics
  • Synovial Membrane / pathology*
  • Tumor Necrosis Factor-alpha / adverse effects*

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • Interleukin-6
  • Lipoxygenase Inhibitors
  • RNA, Small Interfering
  • Tumor Necrosis Factor-alpha
  • Leukotriene B4
  • Arachidonate 5-Lipoxygenase
  • CHUK protein, human
  • I-kappa B Kinase
  • IKBKB protein, human

Grants and funding

The work was supported by a grant from National Science Council (NSC 102-2314-B-002-045-MY3). RNAi reagents were obtained from the National RNAi Core Facility located at the Institute of Molecular Biology/Genomic Research Center, Academia Sinica. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.