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Inflammasome activators induce fibronectin expression and release in macrophages
Hye-Kyoung Jun, Young-Jung Jung, Bong-Kyu Choi1,2
1Department of Oral Microbiology and Immunology, School of Dentistry, Seoul National University, Jongno-gu, Seoul, South Korea.
Cellular Microbiology
|November 22, 2016
Summary
Extracellular fibronectin (Fn) amplifies inflammasome activation and inflammatory cell death. Pathogen activators induce Fn secretion, while plasma Fn triggers caspase-1 activation and death in various cells.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Extracellular fibronectin (Fn) acts as an endogenous danger signal, activating pro-inflammatory pathways.
- Fn is a potential biomarker for various diseases due to its role in inflammation.
Purpose of the Study:
- To investigate the role of fibronectin in inflammasome-mediated inflammatory responses.
- To elucidate the mechanism by which pathogen-derived activators influence Fn expression and secretion.
Main Methods:
- Macrophage culture and stimulation with pathogen-derived activators.
- Assessment of fibronectin expression and secretion.
- Analysis of caspase-1 activation and cell death pathways.
- Treatment of various cell types with plasma fibronectin.
Main Results:
- Pathogen activators induce fibronectin expression and secretion in macrophages via ATP and caspase-1.
- Plasma fibronectin triggers caspase-1 activation and cell death in macrophages, epithelial cells, and fibroblasts.
- Fibronectin amplifies inflammasome-activated caspase-1 signaling and promotes inflammatory cell death.
Conclusions:
- Fibronectin plays a significant role in amplifying inflammation and cell death downstream of inflammasome activation.
- Fn is a key mediator in cellular responses to inflammatory triggers.
- These findings highlight fibronectin's critical involvement in disease pathogenesis.
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