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Particulate Matter Induces NLRP3 Inflammasome-Mediated Pyroptosis in Human Nasal Epithelial Cells
Hosung Choi1, Hyunsu Choi2, Jeong-Min Oh2
1Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Journal of Rhinology : Official Journal of the Korean Rhinologic Society
|December 12, 2024
Summary
Particulate matter (PM) exposure triggers pyroptosis, a form of cell death, in human nasal epithelial cells. This process is dependent on the NLRP3 inflammasome signaling pathway.
Area of Science:
- Environmental Health
- Cell Biology
- Immunology
Background:
- Air pollution, specifically particulate matter (PM), poses significant health risks.
- PM exposure is known to induce cell death, including pyroptosis.
- Limited research exists on PM-induced pyroptosis in nasal epithelial cells.
Purpose of the Study:
- To investigate the effects of PM on human nasal epithelial cells.
- To explore the mechanism of PM-induced pyroptosis in these cells.
Main Methods:
- Human nasal epithelial cells were cultured in vitro.
- Cell viability, death (LDH release, PI staining), and pyroptosis markers (NLRP3, caspase-1, GSDMD-N, IL-1β, IL-18) were assessed.
- The role of the NLRP3 inflammasome was investigated using MCC950 inhibition.
Main Results:
- PM exposure decreased cell viability and increased cell death markers.
- Elevated expression of pyroptosis-related proteins (NLRP3, cleaved caspase-1, GSDMD-N) and cytokines (IL-1β, IL-18) was observed.
- Inhibition of the NLRP3 inflammasome attenuated PM-induced pyroptosis.
Conclusions:
- Particulate matter triggers pyroptosis in human nasal epithelial cells.
- The NLRP3 inflammasome-dependent signaling pathway is crucial in PM-induced pyroptosis.
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