Carbon nanoparticles adversely affect CFTR expression and toxicologically relevant pathways

Area of Science:

• Environmental Health
• Cell Biology
• Respiratory Medicine

Background:

• Cystic fibrosis (CF) is a genetic disorder caused by CFTR gene mutations, leading to respiratory failure.
• Ultrafine carbonaceous particles from air pollution are a growing health concern.
• The impact of carbon nanoparticles (CNP) on CFTR expression in lung cells was previously unknown.

Purpose of the Study:

• To investigate the effects of spark-ablated carbon nanoparticles (CNP) on CFTR expression in human bronchial epithelial cells.
• To assess the cellular and molecular responses of lung cells to CNP exposure.

Main Methods:

• Human bronchial epithelial cells (16HBE14o-) were cultured under air-liquid interface (ALI) conditions.
• Cells were exposed to spark-ablated CNP for 4 hours.
• CFTR expression, epithelial barrier integrity, and transcriptomic profiles were analyzed.

Main Results:

• ALI-cultured cells showed good barrier integrity and elevated CFTR expression prior to exposure.
• CNP exposure decreased epithelial barrier integrity and reduced both CFTR transcript and protein levels.
• Transcriptomic analysis indicated that CNP exposure induced oxidative stress, apoptosis, and DNA damage.

Conclusions:

• Spark-ablated carbon nanoparticles reduce CFTR expression in lung epithelial cells.
• CNP exposure triggers cellular stress responses including oxidative stress, apoptosis, and DNA damage.
• These findings highlight a potential mechanism by which air pollution exacerbates respiratory conditions like cystic fibrosis.