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Lipopolysaccharide-Binding Protein Downregulates Fractalkine through Activation of p38 MAPK and NF-κB

Xia Huang1,2, Yi Zeng3, Yujie Jiang1,2

  • 1The First Clinical Medical College of Jinan University, Guangzhou, Guangdong Province 510630, China.

Mediators of Inflammation
|June 22, 2017
PubMed
Abstract

Insights

Lipopolysaccharide (LPS) increases lipopolysaccharide-binding protein (LBP) and decreases fractalkine in acute respiratory distress syndrome (ARDS). LBP activation of p38 MAPK and NF-κB pathways downregulates fractalkine, contributing to ARDS pathogenesis.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Molecular Biology

Background:

  • Lipopolysaccharide-binding protein (LBP) and fractalkine are implicated in acute respiratory distress syndrome (ARDS) pathogenesis.
  • This study investigates the interplay between LBP and fractalkine in lipopolysaccharide (LPS)-induced ARDS models.

Purpose of the Study:

  • To elucidate the regulatory role of LBP in fractalkine expression within LPS-induced cellular and animal models of ARDS.
  • To explore the involvement of p38 MAPK and p65 NF-κB signaling pathways in LBP-mediated fractalkine modulation.

Main Methods:

  • Utilized A549 cells and an LPS-induced ARDS rat model.
  • Employed techniques including RT-PCR, western blotting, ELISA, immunofluorescence, co-immunoprecipitation, and immunohistochemistry.
  • Investigated the effects of LBP manipulation (overexpression, silencing) and pathway inhibitors (SB203580, SC-514) on fractalkine, LBP, p38 MAPK, and p65 NF-κB.

Main Results:

  • LPS treatment upregulated LBP and downregulated fractalkine in both A549 cells and rat lungs.
  • LBP overexpression exacerbated fractalkine downregulation, while LBP silencing, SB203580, and SC-514 reversed this effect.
  • In vivo, LBPK95A, SB203580, and SC-514 treatments attenuated lung injury and normalized fractalkine levels by inhibiting phospho-p38 MAPK and p65 NF-κB.

Conclusions:

  • LBP downregulates fractalkine expression in LPS-induced ARDS.
  • This downregulation is mediated through the activation of p38 MAPK and NF-κB signaling pathways.
  • Targeting LBP or these pathways may offer therapeutic strategies for ARDS.

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