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The expression of fibronectin is significantly suppressed in macrophages to exert a protective effect against
Hong-Yi Chen1, Mei-Hui Lin1,2,3, Chien-Cheng Chen4
1Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, No. 259, Wenhua 1st Road, Guishan, Taoyuan, 333, Taiwan.
Background:
Fibronectin (Fn) plays a major role in the attachment of Staphylococcus aureus to host cells by bridging staphylococcal fibronectin-binding proteins (FnBPs) and cell-surface integrins. A previous study demonstrated that the phagocytosis of S. aureus by macrophages is enhanced in the presence of exogenous Fn. We recently found that FnBPs overexpression also enhances phagocytic activity. The effect of S. aureus infection on the expression of macrophage Fn was investigated.
Result:
The level of Fn secreted by monocytes (THP-1), macrophages, human lung adenocarcinoma (A549) cells, and hepatocellular carcinoma (HepG2) cells in response to S. aureus infection was determined by Western blotting and it was significantly suppressed only in macrophages. The activation of signaling pathways associated with Fn regulation in macrophages and HepG2 cells was also investigated by Western blotting. Erk was activated in both macrophages and HepG2 cells, whereas Src-JNK-c-Jun signaling was only activated in macrophages. A significant decrease in macrophage viability was observed in response to S. aureus infection in the presence of exogenous Fn.
Conclusion:
The Src-JNK-c-Jun signaling pathway was activated in macrophages in response to S. aureus infection and resulted in the suppression of Fn expression. This suppression may play a protective role in macrophages against S. aureus infection. This study provides the first demonstration that Fn is suppressed in macrophages by S. aureus infection.
Insights
Staphylococcus aureus infection suppresses fibronectin (Fn) expression in macrophages via Src-JNK-c-Jun signaling. This Fn suppression may protect macrophages during S. aureus infection.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Fibronectin (Fn) mediates Staphylococcus aureus (S. aureus) attachment to host cells via fibronectin-binding proteins (FnBPs) and integrins.
- Previous research indicated that exogenous Fn enhances S. aureus phagocytosis by macrophages.
- Our recent findings show FnBPs overexpression also boosts phagocytic activity.
Purpose of the Study:
- To investigate the impact of S. aureus infection on fibronectin expression in macrophages.
- To elucidate the signaling pathways involved in fibronectin regulation during S. aureus infection.
Main Methods:
- Western blotting was used to quantify fibronectin secretion in response to S. aureus infection across various cell types (monocytes, macrophages, A549, HepG2).
- Signaling pathway activation (Erk, Src-JNK-c-Jun) was assessed in macrophages and HepG2 cells.
- Macrophage viability was evaluated in the presence of exogenous fibronectin and S. aureus.
Main Results:
- S. aureus infection significantly suppressed fibronectin secretion specifically in macrophages.
- Erk signaling was activated in both macrophages and HepG2 cells.
- Src-JNK-c-Jun signaling was exclusively activated in macrophages, correlating with fibronectin suppression.
- Macrophage viability decreased when exposed to S. aureus and exogenous fibronectin.
Conclusions:
- Activation of the Src-JNK-c-Jun pathway in macrophages during S. aureus infection leads to fibronectin expression suppression.
- This fibronectin suppression by S. aureus may confer a protective effect on macrophages.
- This study is the first to demonstrate fibronectin suppression in macrophages in response to S. aureus infection.