Resveratrol Attenuates Staphylococcus Aureus-Induced Monocyte Adhesion through Downregulating PDGFR/AP-1 Activation

I-Ta Lee1,2, Chih-Chung Lin3, Chien-Chung Yang4,5

  • 1Department of Medical Research, Taichung Veterans General Hospital, Taichung 407, Taiwan. itl700128@gmail.com.

Insights

Resveratrol suppresses Staphylococcus aureus (S. aureus) induced inflammation by inhibiting vascular cell adhesion molecule-1 (VCAM-1) expression and key signaling pathways in lung epithelial cells and mice.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Staphylococcus aureus (S. aureus) is a common pathogen causing pneumonia and septicemia.
  • S. aureus infection is associated with upregulation of cell adhesion molecules, contributing to inflammation.
  • Resveratrol, a natural antioxidant, exhibits anti-inflammatory and immune-modulating properties.

Purpose of the Study:

  • To investigate the inhibitory effects of resveratrol on S. aureus-induced inflammation.
  • To elucidate the molecular mechanisms underlying resveratrol's anti-inflammatory action in S. aureus infection.

Main Methods:

  • Human lung epithelial cells (HPAEpiCs) and a mouse model of S. aureus infection were used.
  • VCAM-1 expression, leukocyte count, and phosphorylation of signaling proteins (c-Src, PDGFR, p38 MAPK, JNK1/2) were assessed.
  • THP-1 cell adhesion and transcription factor activation (c-Jun, ATF2) were analyzed.

Main Results:

  • Resveratrol inhibited S. aureus-induced VCAM-1 expression in HPAEpiCs.
  • Resveratrol reduced S. aureus-enhanced leukocyte count in mouse bronchoalveolar lavage fluid.
  • Resveratrol suppressed S. aureus-stimulated phosphorylation of c-Src, PDGFR, p38 MAPK, JNK1/2, and activation of c-Jun and ATF2.

Conclusions:

  • Resveratrol effectively suppresses S. aureus-induced inflammatory signaling.
  • Resveratrol inhibits VCAM-1 expression and inflammatory cell adhesion.
  • Resveratrol acts by diminishing key signaling pathways including c-Src, PDGFR, MAPK, JNK, and AP-1 activation.

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