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Overexpression of BPIFB4 Alleviates COPD Inflammatory Damage by Inhibiting M1 Macrophage Activation via the PI3K/AKT

Lexin Xue1,2, Jingran Xu3, Hui Gong4

  • 1Department of Respiratory and Critical Care Medicine, First People's Hospital of Kashgar, Kashgar, Xinjiang, China.

Lung
|June 16, 2025
PubMed
Abstract

Insights

BPI Fold-Containing Family B Member 4 (BPIFB4) overexpression reduces M1 macrophage polarization via the PI3K-AKT1 pathway, alleviating lung damage in COPD. Silencing BPIFB4 worsens inflammation and COPD progression.

Area of Science:

  • Immunology
  • Pulmonology
  • Molecular Biology

Background:

  • Macrophage polarization is critical for managing inflammation in Chronic Obstructive Pulmonary Disease (COPD).
  • The specific role of BPI Fold-Containing Family B Member 4 (BPIFB4) in COPD pathogenesis requires further investigation.
  • Understanding BPIFB4's impact on macrophage polarization is key to developing novel COPD therapeutics.

Purpose of the Study:

  • To investigate how BPIFB4 influences macrophage polarization.
  • To elucidate the role of the phosphoinositide 3-kinase (PI3K)-AKT1 signaling pathway in BPIFB4-mediated macrophage modulation.
  • To determine the therapeutic potential of BPIFB4 in COPD.

Main Methods:

  • Utilized a COPD mouse model induced by cigarette smoke (CS) and lipopolysaccharide (LPS), alongside CSE-treated THP-1 cells.
  • Manipulated BPIFB4 expression (overexpression and silencing) and assessed its effects on macrophage polarization (M1/M2) and inflammatory markers.
  • Analyzed the activation of the PI3K-AKT1 pathway using qPCR, Western blots, and flow cytometry.

Main Results:

  • BPIFB4 gene silencing exacerbated lung damage and increased M1 macrophage polarization and pro-inflammatory cytokines.
  • BPIFB4 overexpression in COPD models significantly activated the PI3K-AKT1 pathway, reducing M1 macrophages and associated inflammation.
  • Inhibition of the PI3K-AKT1 pathway reversed the protective effects of BPIFB4, increasing M1 polarization and cytokine levels.

Conclusions:

  • BPIFB4 overexpression mitigates M1 macrophage polarization through PI3K-AKT1 pathway activation.
  • This modulation by BPIFB4 reduces lung tissue damage and dysfunction in COPD.
  • BPIFB4 represents a potential therapeutic target for managing COPD-related inflammation.
Keywords:
BPIFB4COPDMacrophagesPI3K-AKT1Polarization

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