Indoor pollution induced oxinflammatory responses in lung tissues

Area of Science:

• Environmental Health
• Cell Biology
• Toxicology

Background:

• Indoor particulate matter (PM) exposure is linked to impaired redox metabolism and inflammation, potentially worsening respiratory conditions.
• Lung epithelial cells are key players, releasing inflammatory and oxidative stress mediators after PM uptake.

Purpose of the Study:

• To investigate the mechanisms of redox metabolism disruption and NLRP3 inflammasome activation in lung cells exposed to indoor dust (ID).

Main Methods:

• Exposure of A549 cells and EpiAlveolar 3D tissue models to ID (25 and 100 μg/mL) for up to 24 hours.
• Analysis of particle uptake via TEM, intracellular oxidative stress, lipid peroxidation (4-HNE), NF-κB translocation, and inflammasome activation (NLRP3, ASC, IL-1β).
• Assessment of A549 cell wound closure and EpiAlveolar barrier integrity (TEER), HO-1 expression.

Main Results:

• ID particles were observed within cells; increased intracellular oxidative stress and lipid damage (4-HNE) were detected.
• Dose- and time-dependent NF-κB translocation and NLRP3 inflammasome activation (NLRP3, ASC, IL-1β) were evidenced.
• Impaired wound closure in A549 cells and compromised barrier integrity in the 3D model, with elevated HO-1 and 4-HNE.

Conclusions:

• ID exposure induces oxidative stress and inflammation in lung tissues via NLRP3 inflammasome activation.
• These cellular changes contribute to impaired lung cell function and barrier integrity, highlighting ID as a risk factor for respiratory diseases.