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PM2.5 induces inflammatory responses via oxidative stress-mediated mitophagy in human bronchial epithelial cells
Xuedi Zhai1, Jianshu Wang2, Jiaojiao Sun1
1School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou 215123, Jiangsu, China.
Background:
Fine particulate matter (PM2.5) is a ubiquitous air pollutant, and it has been reported to be closely associated with lung inflammatory injury. In this study, the potential molecular mechanisms underlying PM2.5-induced cellular inflammation in human bronchial epithelial (BEAS-2B) cells were investigated.
Materials And Methods:
Ambient PM2.5 particulates from Suzhou, China, were collected and re-suspended in ultrapure water. Cellular damages, characterized by oxidative stress, mitochondrial injury, and inflammatory cytokine production, were determined in 24 h PM2.5-treated BEAS-2B cells with or without 3-methyladenine (3-MA; autophagy inhibitor) pretreatment. Biomarkers related to oxidative damage, inflammatory injury and autophagy signaling pathways were also measured.
Results:
Uptake of PM2.5 in BEAS-2B cells induced cellular oxidative damage, mitochondrial injury, and inflammatory responses as indicated by a significant decrease in GSH/GSSG ratio, increased MDA content, dilated mitochondria with loss and rupture of crista, and production of inflammatory cytokines. Activation of Nrf-2/TXNIP-mediated NF-κB and Bnip3L/NIX-dependent mitophagy signaling pathways, as well as accumulation of autophagosomes and autolysosomes, were also observed. A 6 h pretreatment of 3-MA increased PM2.5-induced oxidative damage and cellular inflammation as indicated by increasing protein levels of HO-1, TXNIP, Bnip3L/NIX and IL-8 gene expression.
Conclusions:
PM2.5 induced cellular inflammatory injury by oxidative stress, mitochondrial dysfunction, and mitophagy initiation. Although induction of Bnip3L/NIX-mediated mitophagy in BEAS-2B cells appeared to confer protection in response to PM2.5, dysfunction of autophagic flux may be a critical contributor to defective mitophagy and cellular inflammatory response.
Insights
Fine particulate matter (PM2.5) causes lung inflammation through oxidative stress and mitochondrial damage. Autophagy, particularly mitophagy, plays a role, but its dysfunction may worsen PM2.5-induced cellular injury.
Area of Science:
- Environmental Health
- Cell Biology
- Toxicology
Background:
- Fine particulate matter (PM2.5) is a widespread air pollutant linked to lung inflammation.
- Human bronchial epithelial cells (BEAS-2B) are a relevant model for studying PM2.5 effects.
- Understanding PM2.5's molecular mechanisms in lung cells is crucial for public health.
Purpose of the Study:
- Investigate the molecular mechanisms of PM2.5-induced inflammation in BEAS-2B cells.
- Examine the roles of oxidative stress, mitochondrial injury, and autophagy in PM2.5 toxicity.
- Assess the impact of autophagy inhibition on PM2.5-induced cellular damage.
Main Methods:
- BEAS-2B cells were exposed to PM2.5 with or without autophagy inhibitor 3-methyladenine (3-MA).
- Assessed cellular damage markers: oxidative stress (GSH/GSSG, MDA), mitochondrial integrity, and inflammatory cytokines (IL-8).
- Measured signaling pathways: Nrf-2/TXNIP/NF-κB and Bnip3L/NIX-dependent mitophagy.
Main Results:
- PM2.5 exposure induced oxidative stress, mitochondrial damage, and inflammation in BEAS-2B cells.
- Activation of Nrf-2/TXNIP and Bnip3L/NIX mitophagy pathways was observed.
- 3-MA pretreatment exacerbated PM2.5-induced oxidative damage and inflammation.
Conclusions:
- PM2.5 triggers lung cell injury via oxidative stress, mitochondrial dysfunction, and mitophagy.
- Bnip3L/NIX-mediated mitophagy may offer protection against PM2.5 toxicity.
- Impaired autophagic flux could contribute to PM2.5-induced cellular inflammation.
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