Resveratrol attenuates staphylococcus aureus-induced monocyte adhesion through downregulating pdgfr/ap-1 activation in human lung epithelial cells

I-Ta Lee, Chih Chung Lin, Chien Chung Yang, Li Der Hsiao, Ming Yen Wu, Chuen Mao Yang

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Staphylococcus aureus (S. aureus) is a very common Gram-positive bacterium. It is widely distributed in air, soil, and water. S. aureus often causes septicemia and pneumonia in patients. In addition, it is considered to play a key role in mediating cell adhesion molecules upregulation. Resveratrol is a natural antioxidant with diverse biological effects, including the modulation of immune function, anti-inflammation, and cancer chemoprevention. In this study, we proved that S. aureus-upregulated vascular cell adhesion molecule-1 (VCAM-1) expression in human lung epithelial cells (HPAEpiCs) was inhibited by resveratrol. We also observed that resveratrol downregulated S. aureus-enhanced leukocyte count in bronchoalveolar lavage (BAL) fluid in mice. In HPAEpiCs, S. aureus stimulated c-Src, PDGFR, p38 MAPK, or JNK1/2 phosphorylation, which was inhibited by resveratrol. S. aureus induced the adhesion of THP-1 cells (a human monocytic cell line) to HPAEpiCs, which was also reduced by resveratrol. Finally, we found that S. aureus induced c-Src/PDGFR/p38 MAPK and JNK1/2-dependent c-Jun and ATF2 activation and in vivo binding of c-Jun and ATF2 to the VCAM-1 promoter, which were inhibited by resveratrol. Thus, resveratrol functions as a suppressor of S. aureus-induced inflammatory signaling, not only by inhibiting VCAM-1 expression but also by diminishing c-Src, PDGFR, JNK1/2, p38 MAPK, and AP-1 activation in HPAEpiCs.

Original languageEnglish
Article number3058
JournalInternational Journal of Molecular Sciences
Volume19
Issue number10
DOIs
Publication statusPublished - Jan 1 2018
Externally publishedYes

Fingerprint

Resveratrol
monocytes
staphylococcus
lungs
Staphylococcus aureus
Monocytes
adhesion
Down-Regulation
Adhesion
Epithelial Cells
Chemical activation
activation
Cell adhesion
Lung
Vascular Cell Adhesion Molecule-1
p38 Mitogen-Activated Protein Kinases
Molecules
cells
molecules
Phosphorylation

Keywords

  • Ap-1
  • Lung inflammation
  • Resveratrol
  • Signaling pathways
  • Staphylococcus aureus

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

Resveratrol attenuates staphylococcus aureus-induced monocyte adhesion through downregulating pdgfr/ap-1 activation in human lung epithelial cells. / Lee, I-Ta; Lin, Chih Chung; Yang, Chien Chung; Hsiao, Li Der; Wu, Ming Yen; Yang, Chuen Mao.

In: International Journal of Molecular Sciences, Vol. 19, No. 10, 3058, 01.01.2018.

Research output: Contribution to journalArticle

@article{5eb014b66cc24a2f93b28980a49d1fbd,
title = "Resveratrol attenuates staphylococcus aureus-induced monocyte adhesion through downregulating pdgfr/ap-1 activation in human lung epithelial cells",
abstract = "Staphylococcus aureus (S. aureus) is a very common Gram-positive bacterium. It is widely distributed in air, soil, and water. S. aureus often causes septicemia and pneumonia in patients. In addition, it is considered to play a key role in mediating cell adhesion molecules upregulation. Resveratrol is a natural antioxidant with diverse biological effects, including the modulation of immune function, anti-inflammation, and cancer chemoprevention. In this study, we proved that S. aureus-upregulated vascular cell adhesion molecule-1 (VCAM-1) expression in human lung epithelial cells (HPAEpiCs) was inhibited by resveratrol. We also observed that resveratrol downregulated S. aureus-enhanced leukocyte count in bronchoalveolar lavage (BAL) fluid in mice. In HPAEpiCs, S. aureus stimulated c-Src, PDGFR, p38 MAPK, or JNK1/2 phosphorylation, which was inhibited by resveratrol. S. aureus induced the adhesion of THP-1 cells (a human monocytic cell line) to HPAEpiCs, which was also reduced by resveratrol. Finally, we found that S. aureus induced c-Src/PDGFR/p38 MAPK and JNK1/2-dependent c-Jun and ATF2 activation and in vivo binding of c-Jun and ATF2 to the VCAM-1 promoter, which were inhibited by resveratrol. Thus, resveratrol functions as a suppressor of S. aureus-induced inflammatory signaling, not only by inhibiting VCAM-1 expression but also by diminishing c-Src, PDGFR, JNK1/2, p38 MAPK, and AP-1 activation in HPAEpiCs.",
keywords = "Ap-1, Lung inflammation, Resveratrol, Signaling pathways, Staphylococcus aureus",
author = "I-Ta Lee and Lin, {Chih Chung} and Yang, {Chien Chung} and Hsiao, {Li Der} and Wu, {Ming Yen} and Yang, {Chuen Mao}",
year = "2018",
month = "1",
day = "1",
doi = "10.3390/ijms19103058",
language = "English",
volume = "19",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "MDPI AG",
number = "10",

}

TY - JOUR

T1 - Resveratrol attenuates staphylococcus aureus-induced monocyte adhesion through downregulating pdgfr/ap-1 activation in human lung epithelial cells

AU - Lee, I-Ta

AU - Lin, Chih Chung

AU - Yang, Chien Chung

AU - Hsiao, Li Der

AU - Wu, Ming Yen

AU - Yang, Chuen Mao

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Staphylococcus aureus (S. aureus) is a very common Gram-positive bacterium. It is widely distributed in air, soil, and water. S. aureus often causes septicemia and pneumonia in patients. In addition, it is considered to play a key role in mediating cell adhesion molecules upregulation. Resveratrol is a natural antioxidant with diverse biological effects, including the modulation of immune function, anti-inflammation, and cancer chemoprevention. In this study, we proved that S. aureus-upregulated vascular cell adhesion molecule-1 (VCAM-1) expression in human lung epithelial cells (HPAEpiCs) was inhibited by resveratrol. We also observed that resveratrol downregulated S. aureus-enhanced leukocyte count in bronchoalveolar lavage (BAL) fluid in mice. In HPAEpiCs, S. aureus stimulated c-Src, PDGFR, p38 MAPK, or JNK1/2 phosphorylation, which was inhibited by resveratrol. S. aureus induced the adhesion of THP-1 cells (a human monocytic cell line) to HPAEpiCs, which was also reduced by resveratrol. Finally, we found that S. aureus induced c-Src/PDGFR/p38 MAPK and JNK1/2-dependent c-Jun and ATF2 activation and in vivo binding of c-Jun and ATF2 to the VCAM-1 promoter, which were inhibited by resveratrol. Thus, resveratrol functions as a suppressor of S. aureus-induced inflammatory signaling, not only by inhibiting VCAM-1 expression but also by diminishing c-Src, PDGFR, JNK1/2, p38 MAPK, and AP-1 activation in HPAEpiCs.

AB - Staphylococcus aureus (S. aureus) is a very common Gram-positive bacterium. It is widely distributed in air, soil, and water. S. aureus often causes septicemia and pneumonia in patients. In addition, it is considered to play a key role in mediating cell adhesion molecules upregulation. Resveratrol is a natural antioxidant with diverse biological effects, including the modulation of immune function, anti-inflammation, and cancer chemoprevention. In this study, we proved that S. aureus-upregulated vascular cell adhesion molecule-1 (VCAM-1) expression in human lung epithelial cells (HPAEpiCs) was inhibited by resveratrol. We also observed that resveratrol downregulated S. aureus-enhanced leukocyte count in bronchoalveolar lavage (BAL) fluid in mice. In HPAEpiCs, S. aureus stimulated c-Src, PDGFR, p38 MAPK, or JNK1/2 phosphorylation, which was inhibited by resveratrol. S. aureus induced the adhesion of THP-1 cells (a human monocytic cell line) to HPAEpiCs, which was also reduced by resveratrol. Finally, we found that S. aureus induced c-Src/PDGFR/p38 MAPK and JNK1/2-dependent c-Jun and ATF2 activation and in vivo binding of c-Jun and ATF2 to the VCAM-1 promoter, which were inhibited by resveratrol. Thus, resveratrol functions as a suppressor of S. aureus-induced inflammatory signaling, not only by inhibiting VCAM-1 expression but also by diminishing c-Src, PDGFR, JNK1/2, p38 MAPK, and AP-1 activation in HPAEpiCs.

KW - Ap-1

KW - Lung inflammation

KW - Resveratrol

KW - Signaling pathways

KW - Staphylococcus aureus

UR - http://www.scopus.com/inward/record.url?scp=85054772850&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85054772850&partnerID=8YFLogxK

U2 - 10.3390/ijms19103058

DO - 10.3390/ijms19103058

M3 - Article

C2 - 30301269

AN - SCOPUS:85054772850

VL - 19

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 10

M1 - 3058

ER -